Examples of healthy lifelong asymptomatic carrier of a severe infectious disease?

Examples of healthy lifelong asymptomatic carrier of a severe infectious disease?

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I am curious, is there any known disease/infection that is very severe normally (patient suffers greatly and die easily without medical treatment), but ends up having little to no effect on the lives of asymptomatic carriers? I am asking this as I am thinking whether this means certain disease symptoms are mechanisms resulted from evolution to protect the "greater good", i.e. killing the patient to avoid transmission to another member of the species.

I am curious, is there any known disease/infection that is very severe normally, but ends up having little to no effect on the lives of asymptomatic carriers?

HIV is an obvious example, where so-called "long-term nonprogressors" successfully suppress HIV replication sufficiently that they do not develop AIDS but are unable to clear the infection entirely [1].

patient suffers greatly and die easily without medical treatment

Since the comments below seem to suggest that HIV does not cause death without medical treatment, I'll point out that this is incorrect. Over 30 million people have died from HIV infection.

I am asking this as I am thinking whether this means certain disease symptoms are evolutionarily wired to protect the "greater good"

It does not. Selection happens on individuals and not whole species, so the greater good is irrelevant. Asymptomatic infection is a point on the spectrum of possible responses to infection between sterilizing immunity and death. Individuals who are chronically infected mount enough of an immune response to control the infection but not enough to completely clear it. In the case of HIV, they are typically people who have exceptionally strong immune responses to a normally lethal virus.


The comments below suggest a deep misunderstanding of evolution. Since I think these are really the core of your question, I'll address them here.

If traits really evolve only according to how much an individual reproduce sucessfully, it would be a different world today.

Which individuals reproduce is the sole determinant of which genes are passed down to the next generation. This is because the genetics of each individual are determined at conception, and cannot be changed. Hence, reproduction alone determines the traits of the next generation.

To quote wikipedia[2]:

Evolution is change in the heritable characteristics of biological populations over successive generations. These characteristics are the expressions of genes that are passed on from parent to offspring during reproduction. Different characteristics tend to exist within any given population as a result of mutation, genetic recombination and other sources of genetic variation. Evolution occurs when evolutionary processes such as natural selection (including sexual selection) and genetic drift act on this variation, resulting in certain characteristics becoming more common or rare within a population

Evolution is the process by which some traits are passed down to the next generation while others are not though the mechanisms of selection (e.g. individuals with harmful traits dying) and genetic drift (e.g. random chance).

Thank about a hypothetical super fast reproducing bacteria, using up all resources, which means extinction at the end, such traits would not be passed on. In fact some sort of "moderation" mechanism is needed to take care of the "greater good".

This is exactly what happens if you put a lot of fast reproducing bacteria in a closed environment with limited resources. They will all eventually die.

You seem to be thinking of evolution as something that intelligently looks out for the wellbeing of species. This is not the case. Evolution is a random process by which different amounts of reproduction and survival between individuals alters the composition of the succeeding generations. As a random, emergent process it has no goals, no intelligence, and no sense of "good". Rather, it simply happens as a result of individuals reproducing. This frequently does lead to extinction, as evidenced by the fact that the vast majority of species no longer exist.


"Yes" is the simple answer to the first part of your question. HIV, "Typhoid Mary", maybe Covid19, and other examples have been given.

The second part of your question,

I am asking this as I am thinking whether this means certain disease symptoms are mechanisms resulted from evolution to protect the "greater good", i.e. killing the patient to avoid transmission to another member of the species.

is good, but doesn't have a definite answer as far as I know. However, your idea is certainly plausible. Although displaying symptoms (e.g., a rash, cough, odd behavior, or bad odor) will not benefit the individual, it will benefit individuals who are repelled by those symptoms. In cases where individuals who have a tendency to be repelled by the symptoms also have a tendency to display those symptoms (and those tendencies are encoded genetically), close relatives of those individuals have a distinct selective advantage over other individuals in the population who do not have a tendency to be repelled.

A lot of literature relating to this idea can be found by searching "evolution of altruism" and "kin selection".

Science Brief: COVID-19 Vaccines and Vaccination

COVID-19 vaccination is a critical prevention measure to help end the COVID-19 pandemic. COVID-19 vaccines are now more widely accessible in the United States, and all people 12 years and older are recommended to be vaccinated against COVID-19. Three COVID-19 vaccines are currently authorized by the U.S. Food and Drug Administration (FDA) for emergency use: two mRNA vaccines (Pfizer-BioNTech, Moderna) and one viral vector vaccine (Johnson & Johnson/Janssen vaccine). People are considered fully vaccinated if they are &ge2 weeks following receipt of the second dose in a 2-dose series (mRNA vaccines), or &ge2 weeks following receipt of a single-dose vaccine (Johnson & Johnson/Janssen).*

Public health recommendations for people fully vaccinated with COVID-19 vaccines must consider the evidence, including vaccine effectiveness against symptomatic and asymptomatic COVID-19, as well as vaccine impact on SARS-CoV-2 transmission. Other individual and societal factors are also important when evaluating the benefits and potential harms of prevention measures among vaccinated individuals. The Advisory Committee on Immunization Practices and CDC routinely consider factors such as population values, acceptability, and feasibility of implementation when making vaccine recommendations.(1) These factors were also considered when developing CDC&rsquos interim public health recommendations for fully vaccinated people.

In this scientific brief, we summarize evidence available through May 19, 2021, for the currently authorized COVID-19 vaccines (administered according to the recommended schedules) and additional considerations used to inform public health recommendations for fully vaccinated people, including:

  • Vaccine efficacy and effectiveness against SARS-CoV-2 infection
  • Vaccine performance against emerging SARS-CoV-2 variant viruses
  • Impact of other prevention measures in the context of vaccination

Accumulating evidence indicates that fully vaccinated people without immunocompromising conditions are able to engage in most activities with very low risk of acquiring or transmitting SARS-CoV-2. The benefits of avoiding disruptions such as unnecessary quarantine and social isolation might outweigh the low residual risk of becoming ill with COVID-19, generally with mild disease, or of transmitting the virus to others.

Lesson 1: Introduction to Epidemiology

As described above, the traditional epidemiologic triad model holds that infectious diseases result from the interaction of agent, host, and environment. More specifically, transmission occurs when the agent leaves its reservoir or host through a portal of exit, is conveyed by some mode of transmission, and enters through an appropriate portal of entry to infect a susceptible host. This sequence is sometimes called the chain of infection.

Figure 1.19 Chain of Infection

Source: Centers for Disease Control and Prevention. Principles of epidemiology, 2nd ed. Atlanta: U.S. Department of Health and Human Services1992.


The reservoir of an infectious agent is the habitat in which the agent normally lives, grows, and multiplies. Reservoirs include humans, animals, and the environment. The reservoir may or may not be the source from which an agent is transferred to a host. For example, the reservoir of Clostridium botulinum is soil, but the source of most botulism infections is improperly canned food containing C. botulinum spores.

Human reservoirs. Many common infectious diseases have human reservoirs. Diseases that are transmitted from person to person without intermediaries include the sexually transmitted diseases, measles, mumps, streptococcal infection, and many respiratory pathogens. Because humans were the only reservoir for the smallpox virus, naturally occurring smallpox was eradicated after the last human case was identified and isolated.8

Human reservoirs may or may not show the effects of illness. As noted earlier, a carrier is a person with inapparent infection who is capable of transmitting the pathogen to others. Asymptomatic or passive or healthy carriers are those who never experience symptoms despite being infected. Incubatory carriers are those who can transmit the agent during the incubation period before clinical illness begins. Convalescent carriers are those who have recovered from their illness but remain capable of transmitting to others. Chronic carriers are those who continue to harbor a pathogen such as hepatitis B virus or Salmonella Typhi, the causative agent of typhoid fever, for months or even years after their initial infection. One notorious carrier is Mary Mallon, or Typhoid Mary, who was an asymptomatic chronic carrier of Salmonella Typhi. As a cook in New York City and New Jersey in the early 1900s, she unintentionally infected dozens of people until she was placed in isolation on an island in the East River, where she died 23 years later.(45)

Carriers commonly transmit disease because they do not realize they are infected, and consequently take no special precautions to prevent transmission. Symptomatic persons who are aware of their illness, on the other hand, may be less likely to transmit infection because they are either too sick to be out and about, take precautions to reduce transmission, or receive treatment that limits the disease.

Animal reservoirs. Humans are also subject to diseases that have animal reservoirs. Many of these diseases are transmitted from animal to animal, with humans as incidental hosts. The term zoonosis refers to an infectious disease that is transmissible under natural conditions from vertebrate animals to humans. Long recognized zoonotic diseases include brucellosis (cows and pigs), anthrax (sheep), plague (rodents), trichinellosis/trichinosis (swine), tularemia (rabbits), and rabies (bats, raccoons, dogs, and other mammals). Zoonoses newly emergent in North America include West Nile encephalitis (birds), and monkeypox (prairie dogs). Many newly recognized infectious diseases in humans, including HIV/AIDS, Ebola infection and SARS, are thought to have emerged from animal hosts, although those hosts have not yet been identified.

Environmental reservoirs. Plants, soil, and water in the environment are also reservoirs for some infectious agents. Many fungal agents, such as those that cause histoplasmosis, live and multiply in the soil. Outbreaks of Legionnaires disease are often traced to water supplies in cooling towers and evaporative condensers, reservoirs for the causative organism Legionella pneumophila.

Portal of exit

Portal of exit is the path by which a pathogen leaves its host. The portal of exit usually corresponds to the site where the pathogen is localized. For example, influenza viruses and Mycobacterium tuberculosis exit the respiratory tract, schistosomes through urine, cholera vibrios in feces, Sarcoptes scabiei in scabies skin lesions, and enterovirus 70, a cause of hemorrhagic conjunctivitis, in conjunctival secretions. Some bloodborne agents can exit by crossing the placenta from mother to fetus (rubella, syphilis, toxoplasmosis), while others exit through cuts or needles in the skin (hepatitis B) or blood-sucking arthropods (malaria).

Modes of transmission

An infectious agent may be transmitted from its natural reservoir to a susceptible host in different ways. There are different classifications for modes of transmission. Here is one classification:

  • Direct
    • Direct contact
    • Droplet spread
    • Airborne
    • Vehicleborne
    • Vectorborne (mechanical or biologic)

    In direct transmission, an infectious agent is transferred from a reservoir to a susceptible host by direct contact or droplet spread.

    Direct contact occurs through skin-to-skin contact, kissing, and sexual intercourse. Direct contact also refers to contact with soil or vegetation harboring infectious organisms. Thus, infectious mononucleosis (&ldquokissing disease&rdquo) and gonorrhea are spread from person to person by direct contact. Hookworm is spread by direct contact with contaminated soil.

    Droplet spread refers to spray with relatively large, short-range aerosols produced by sneezing, coughing, or even talking. Droplet spread is classified as direct because transmission is by direct spray over a few feet, before the droplets fall to the ground. Pertussis and meningococcal infection are examples of diseases transmitted from an infectious patient to a susceptible host by droplet spread.

    Indirect transmission refers to the transfer of an infectious agent from a reservoir to a host by suspended air particles, inanimate objects (vehicles), or animate intermediaries (vectors).

    Airborne transmission occurs when infectious agents are carried by dust or droplet nuclei suspended in air. Airborne dust includes material that has settled on surfaces and become resuspended by air currents as well as infectious particles blown from the soil by the wind. Droplet nuclei are dried residue of less than 5 microns in size. In contrast to droplets that fall to the ground within a few feet, droplet nuclei may remain suspended in the air for long periods of time and may be blown over great distances. Measles, for example, has occurred in children who came into a physician&rsquos office after a child with measles had left, because the measles virus remained suspended in the air.(46)

    Vehicles that may indirectly transmit an infectious agent include food, water, biologic products (blood), and fomites (inanimate objects such as handkerchiefs, bedding, or surgical scalpels). A vehicle may passively carry a pathogen &mdash as food or water may carry hepatitis A virus. Alternatively, the vehicle may provide an environment in which the agent grows, multiplies, or produces toxin &mdash as improperly canned foods provide an environment that supports production of botulinum toxin by Clostridium botulinum.

    Vectors such as mosquitoes, fleas, and ticks may carry an infectious agent through purely mechanical means or may support growth or changes in the agent. Examples of mechanical transmission are flies carrying Shigella on their appendages and fleas carrying Yersinia pestis, the causative agent of plague, in their gut. In contrast, in biologic transmission, the causative agent of malaria or guinea worm disease undergoes maturation in an intermediate host before it can be transmitted to humans (Figure 1.20).

    Portal of entry

    The portal of entry refers to the manner in which a pathogen enters a susceptible host. The portal of entry must provide access to tissues in which the pathogen can multiply or a toxin can act. Often, infectious agents use the same portal to enter a new host that they used to exit the source host. For example, influenza virus exits the respiratory tract of the source host and enters the respiratory tract of the new host. In contrast, many pathogens that cause gastroenteritis follow a so-called &ldquofecal-oral&rdquo route because they exit the source host in feces, are carried on inadequately washed hands to a vehicle such as food, water, or utensil, and enter a new host through the mouth. Other portals of entry include the skin (hookworm), mucous membranes (syphilis), and blood (hepatitis B, human immunodeficiency virus).

    Figure 1.20 Complex Life Cycle of Dracunculus medinensis (Guinea worm)

    Source: Centers for Disease Control and Prevention. Principles of epidemiology, 2nd ed. Atlanta: U.S. Department of Health and Human Services1992.

    The final link in the chain of infection is a susceptible host. Susceptibility of a host depends on genetic or constitutional factors, specific immunity, and nonspecific factors that affect an individual&rsquos ability to resist infection or to limit pathogenicity. An individual&rsquos genetic makeup may either increase or decrease susceptibility. For example, persons with sickle cell trait seem to be at least partially protected from a particular type of malaria. Specific immunity refers to protective antibodies that are directed against a specific agent. Such antibodies may develop in response to infection, vaccine, or toxoid (toxin that has been deactivated but retains its capacity to stimulate production of toxin antibodies) or may be acquired by transplacental transfer from mother to fetus or by injection of antitoxin or immune globulin. Nonspecific factors that defend against infection include the skin, mucous membranes, gastric acidity, cilia in the respiratory tract, the cough reflex, and nonspecific immune response. Factors that may increase susceptibility to infection by disrupting host defenses include malnutrition, alcoholism, and disease or therapy that impairs the nonspecific immune response.

    Implications for public health

    Knowledge of the portals of exit and entry and modes of transmission provides a basis for determining appropriate control measures. In general, control measures are usually directed against the segment in the infection chain that is most susceptible to intervention, unless practical issues dictate otherwise.

    Interventions are directed at:

    • Controlling or eliminating agent at source of transmission
    • Protecting portals of entry
    • Increasing host&rsquos defenses

    For some diseases, the most appropriate intervention may be directed at controlling or eliminating the agent at its source. A patient sick with a communicable disease may be treated with antibiotics to eliminate the infection. An asymptomatic but infected person may be treated both to clear the infection and to reduce the risk of transmission to others. In the community, soil may be decontaminated or covered to prevent escape of the agent.

    Some interventions are directed at the mode of transmission. Interruption of direct transmission may be accomplished by isolation of someone with infection, or counseling persons to avoid the specific type of contact associated with transmission. Vehicleborne transmission may be interrupted by elimination or decontamination of the vehicle. To prevent fecal-oral transmission, efforts often focus on rearranging the environment to reduce the risk of contamination in the future and on changing behaviors, such as promoting handwashing. For airborne diseases, strategies may be directed at modifying ventilation or air pressure, and filtering or treating the air. To interrupt vectorborne transmission, measures may be directed toward controlling the vector population, such as spraying to reduce the mosquito population.

    Some strategies that protect portals of entry are simple and effective. For example, bed nets are used to protect sleeping persons from being bitten by mosquitoes that may transmit malaria. A dentist&rsquos mask and gloves are intended to protect the dentist from a patient&rsquos blood, secretions, and droplets, as well to protect the patient from the dentist. Wearing of long pants and sleeves and use of insect repellent are recommended to reduce the risk of Lyme disease and West Nile virus infection, which are transmitted by the bite of ticks and mosquitoes, respectively.

    Some interventions aim to increase a host&rsquos defenses. Vaccinations promote development of specific antibodies that protect against infection. On the other hand, prophylactic use of antimalarial drugs, recommended for visitors to malaria-endemic areas, does not prevent exposure through mosquito bites, but does prevent infection from taking root.

    Finally, some interventions attempt to prevent a pathogen from encountering a susceptible host. The concept of herd immunity suggests that if a high enough proportion of individuals in a population are resistant to an agent, then those few who are susceptible will be protected by the resistant majority, since the pathogen will be unlikely to &ldquofind&rdquo those few susceptible individuals. The degree of herd immunity necessary to prevent or interrupt an outbreak varies by disease. In theory, herd immunity means that not everyone in a community needs to be resistant (immune) to prevent disease spread and occurrence of an outbreak. In practice, herd immunity has not prevented outbreaks of measles and rubella in populations with immunization levels as high as 85% to 90%. One problem is that, in highly immunized populations, the relatively few susceptible persons are often clustered in subgroups defined by socioeconomic or cultural factors. If the pathogen is introduced into one of these subgroups, an outbreak may occur.

    Exercise 1.9

    Information about dengue fever is provided on the following pages. After studying this information, outline the chain of infection by identifying the reservoir(s), portal(s) of exit, mode(s) of transmission, portal(s) of entry, and factors in host susceptibility.

    1. Reservoirs:
    2. Portals of exit:
    3. Modes of transmission:
    4. Portals of entry:
    5. Factors in host susceptibility:

    Dengue Fact Sheet

    Dengue is an acute infectious disease that comes in two forms: dengue and dengue hemorrhagic fever. The principal symptoms of dengue are high fever, severe headache, backache, joint pains, nausea and vomiting, eye pain, and rash. Generally, younger children have a milder illness than older children and adults.

    Dengue hemorrhagic fever is a more severe form of dengue. It is characterized by a fever that lasts from 2 to 7 days, with general signs and symptoms that could occur with many other illnesses (e.g., nausea, vomiting, abdominal pain, and headache). This stage is followed by hemorrhagic manifestations, tendency to bruise easily or other types of skin hemorrhages, bleeding nose or gums, and possibly internal bleeding. The smallest blood vessels (capillaries) become excessively permeable (&ldquoleaky&rdquo), allowing the fluid component to escape from the blood vessels. This may lead to failure of the circulatory system and shock, followed by death, if circulatory failure is not corrected. Although the average case-fatality rate is about 5%, with good medical management, mortality can be less than 1%.

    Dengue and dengue hemorrhagic fever are caused by any one of four closely related flaviviruses, designated DEN-1, DEN&ndash2, DEN-3, or DEN-4.

    Diagnosis of dengue infection requires laboratory confirmation, either by isolating the virus from serum within 5 days after onset of symptoms, or by detecting convalescent-phase specific antibodies obtained at least 6 days after onset of symptoms.

    What is the treatment for dengue or dengue hemorrhagic fever?

    There is no specific medication for treatment of a dengue infection. Persons who think they have dengue should use analgesics (pain relievers) with acetaminophen and avoid those containing aspirin. They should also rest, drink plenty of fluids, and consult a physician. Persons with dengue hemorrhagic fever can be effectively treated by fluid replacement therapy if an early clinical diagnosis is made, but hospitalization is often required.

    How common is dengue and where is it found?

    Dengue is endemic in many tropical countries in Asia and Latin America, most countries in Africa, and much of the Caribbean, including Puerto Rico. Cases have occurred sporadically in Texas. Epidemics occur periodically. Globally, an estimated 50 to 100 million cases of dengue and several hundred thousand cases of dengue hemorrhagic fever occur each year, depending on epidemic activity. Between 100 and 200 suspected cases are introduced into the United States each year by travelers.

    How is dengue transmitted?

    Dengue is transmitted to people by the bite of an Aedes mosquito that is infected with a dengue virus. The mosquito becomes infected with dengue virus when it bites a person who has dengue or DHF and after about a week can transmit the virus while biting a healthy person. Monkeys may serve as a reservoir in some parts of Asia and Africa. Dengue cannot be spread directly from person to person.

    Who has an increased risk of being exposed to dengue?

    Susceptibility to dengue is universal. Residents of or visitors to tropical urban areas and other areas where dengue is endemic are at highest risk of becoming infected. While a person who survives a bout of dengue caused by one serotype develops lifelong immunity to that serotype, there is no cross-protection against the three other serotypes.

    What can be done to reduce the risk of acquiring dengue?

    There is no vaccine for preventing dengue. The best preventive measure for residents living in areas infested with Aedes aegypti is to eliminate the places where the mosquito lays her eggs, primarily artificial containers that hold water.

    Items that collect rainwater or are used to store water (for example, plastic containers, 55-gallon drums, buckets, or used automobile tires) should be covered or properly discarded. Pet and animal watering containers and vases with fresh flowers should be emptied and scoured at least once a week. This will eliminate the mosquito eggs and larvae and reduce the number of mosquitoes present in these areas.

    For travelers to areas with dengue, as well as people living in areas with dengue, the risk of being bitten by mosquitoes indoors is reduced by utilization of air conditioning or windows and doors that are screened. Proper application of mosquito repellents containing 20% to 30% DEET as the active ingredient on exposed skin and clothing decreases the risk of being bitten by mosquitoes. The risk of dengue infection for international travelers appears to be small, unless an epidemic is in progress.

    Can epidemics of dengue hemorrhagic fever be prevented?

    The emphasis for dengue prevention is on sustainable, community-based, integrated mosquito control, with limited reliance on insecticides (chemical larvicides and adulticides). Preventing epidemic disease requires a coordinated community effort to increase awareness about dengue/DHF, how to recognize it, and how to control the mosquito that transmits it. Residents are responsible for keeping their yards and patios free of sites where mosquitoes can be produced.

    Rates of asymptomatic respiratory virus infection across age groups

    Respiratory viral infections are a leading cause of disease worldwide. A variety of respiratory viruses produce infections in humans with effects ranging from asymptomatic to life-treathening. Standard surveillance systems typically only target severe infections (ED outpatients, hospitalisations, deaths) and fail to track asymptomatic or mild infections. Here we performed a large-scale community study across multiple age groups to assess the pathogenicity of 18 respiratory viruses. We enrolled 214 individuals at multiple New York City locations and tested weekly for respiratory viral pathogens, irrespective of symptom status, from fall 2016 to spring 2018. We combined these test results with participant-provided daily records of cold and flu symptoms and used this information to characterise symptom severity by virus and age category. Asymptomatic infection rates exceeded 70% for most viruses, excepting influenza and human metapneumovirus, which produced significantly more severe outcomes. Symptoms were negatively associated with infection frequency, with children displaying the lowest score among age groups. Upper respiratory manifestations were most common for all viruses, whereas systemic effects were less typical. These findings indicate a high burden of asymptomatic respiratory virus infection exists in the general population.

    Conflict of interest statement

    JS and Columbia University disclose partial ownership of SK Analytics. All other authors declare no competing interests.


    Symptoms by virus. The bars…

    Symptoms by virus. The bars show the fraction of positive results associated with…

    Specific symptoms per (a) virus…

    Specific symptoms per (a) virus and (b) age group. Here infection events (not…

    Distribution of number of illness…

    Distribution of number of illness events (a) and associated symptoms score (b) across…

    A study on infectivity of asymptomatic SARS-CoV-2 carriers

    Background: An ongoing outbreak of coronavirus disease 2019 (COVID-19) has spread around the world. It is debatable whether asymptomatic COVID-19 virus carriers are contagious. We report here a case of the asymptomatic patient and present clinical characteristics of 455 contacts, which aims to study the infectivity of asymptomatic carriers.

    Material and methods: 455 contacts who were exposed to the asymptomatic COVID-19 virus carrier became the subjects of our research. They were divided into three groups: 35 patients, 196 family members and 224 hospital staffs. We extracted their epidemiological information, clinical records, auxiliary examination results and therapeutic schedules.

    Results: The median contact time for patients was four days and that for family members was five days. Cardiovascular disease accounted for 25% among original diseases of patients. Apart from hospital staffs, both patients and family members were isolated medically. During the quarantine, seven patients plus one family member appeared new respiratory symptoms, where fever was the most common one. The blood counts in most contacts were within a normal range. All CT images showed no sign of COVID-19 infection. No severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections was detected in 455 contacts by nucleic acid test.

    Conclusion: In summary, all the 455 contacts were excluded from SARS-CoV-2 infection and we conclude that the infectivity of some asymptomatic SARS-CoV-2 carriers might be weak.

    Keywords: Asymptomatic carrier Contacts Infectivity SARS-CoV-2.

    Copyright © 2020 Elsevier Ltd. All rights reserved.

    Conflict of interest statement

    Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

    Herpes simplex virus type 1 (HSV-1)

    HSV-1 is a highly contagious infection, that is common and endemic throughout the world. Most HSV-1 infections are acquired during childhood, and infection is lifelong. The vast majority of HSV-1 infections are oral herpes (infections in or around the mouth, sometimes called orolabial, oral-labial or oral-facial herpes), but a proportion of HSV-1 infections are genital herpes (infections in the genital or anal area).

    Scope of the problem

    In 2016, an estimated 3.7 billion people under the age of 50, or 67% of the population, had HSV-1 infection (oral or genital). Estimated prevalence of the infection was highest in Africa (88%) and lowest in the Americas (45%).

    With respect to genital HSV-1 infection, between 122 million to 192 million people aged 15-49-years were estimated to have genital HSV-1 infection worldwide in 2016, but prevalence varied substantially by region. Most genital HSV-1 infections are estimated to occur in the Americas, Europe and Western Pacific, where HSV-1 continues to be acquired well into adulthood.

    Signs and symptoms

    Oral herpes infection is mostly asymptomatic, and most people with HSV-1 infection are unaware they are infected. Symptoms of oral herpes include painful blisters or open sores called ulcers in or around the mouth. Sores on the lips are commonly referred to as &ldquocold sores.&rdquo Infected persons will often experience a tingling, itching or burning sensation around their mouth, before the appearance of sores. After initial infection, the blisters or ulcers can periodically recur. The frequency of recurrences varies from person to person.

    Genital herpes caused by HSV-1 can be asymptomatic or can have mild symptoms that go unrecognized. When symptoms do occur, genital herpes is characterised by 1 one or more genital or anal blisters or ulcers. After an initial genital herpes episode, which may can be severe, symptoms may recur. However, genital herpes caused by HSV-1 typically does not recur frequently, unlike genital herpes caused by herpes simplex virus type 2 (HSV-2 see below).


    HSV-1 is mainly transmitted by oral-to-oral contact to cause oral herpes infection, via contact with the HSV-1 virus in sores, saliva, and surfaces in or around the mouth. However, HSV-1 can also be transmitted to the genital area through oral-genital contact to cause genital herpes.

    HSV-1 can be transmitted from oral or skin surfaces that appear normal and when there are no symptoms present. However, the greatest risk of transmission is when there are active sores.

    Individuals who already have HSV-1 oral herpes infection are unlikely to be subsequently infected with HSV-1 in the genital area.

    In rare circumstances, HSV-1 infection can be transmitted from a mother with genital HSV-1 infection to her infant during delivery to cause neonatal herpes (see below).

    Possible complications

    Severe disease

    In immunocompromised people, such as those with advanced HIV infection, HSV-1 can have more severe symptoms and more frequent recurrences. Rarely, HSV-1 infection can also lead to more severe complications such as encephalitis (brain infection) or keratitis (eye infection).

    Neonatal herpes

    Neonatal herpes can occur when an infant is exposed to HSV (HSV-1 or HSV-2) in the genital tract during delivery. Neonatal herpes is rare, occurring in an estimated 10 out of every 100,000 births globally, but is a serious condition that can lead to lasting neurologic disability or death. Women who have genital herpes before they become pregnant are at very low risk of transmitting HSV to their infants. The risk for neonatal herpes is greatest when a mother acquires HSV infection for the first time in late pregnancy., in part because the levels of HSV in the genital tract are highest early in infection.

    Psychosocial impact

    Recurrent symptoms of oral herpes may be uncomfortable and can lead to some social stigma and psychological distress. With genital herpes, these factors can have an important impact on quality of life and sexual relationships. However, in time, most people with either kind of herpes adjust to living with the infection.


    Antiviral medications, such as acyclovir, famciclovir, and valacyclovir, are the most effective medications available for people infected with HSV. These can help to reduce the severity and frequency of symptoms, but cannot cure the infection.


    HSV-1 is most contagious during an outbreak of symptomatic oral herpes, but can also be transmitted when no symptoms are felt or visible. People with active symptoms of oral herpes should avoid oral contact with others and sharing objects that have contact with saliva. They should also abstain from oral sex, to avoid transmitting herpes to the genitals of a sexual partner. Individuals with symptoms of genital herpes should abstain from sexual activity whilst experiencing any of the symptoms.

    People who already have HSV-1 infection are not at risk of getting it again, but they are still at risk of acquiring herpes simplex virus type 2 (HSV-2) genital infection (see below).

    The consistent and correct use of condoms can help to prevent the spread of genital herpes. However, condoms can only reduce the risk of infection, as outbreaks of genital herpes can occur in areas not covered by a condom.

    People who already have HSV-1 infection are not at risk of getting it again, but they are still at risk of acquiring HSV-2 genital infection (see below).

    Pregnant women with symptoms of genital herpes should inform their health care providers. Preventing acquisition of a new genital herpes infection is particularly important for women in late pregnancy, as this is when the risk for neonatal herpes is greatest.

    Additional research is underway to develop more effective prevention methods against HSV infection, such as vaccines. Several candidate HSV vaccines are currently being studied.

    You Probably Have an Asymptomatic Infection Right Now

    No, not COVID-19. Many, many viruses can infect humans without making us sick, and how they do that is one of biology’s deepest mysteries.

    One of the most perplexing and enduring mysteries of the pandemic is also one of the most fundamental questions about viruses. How can the same virus that kills so many go entirely unnoticed in others?

    The mystery is hardly unique to COVID-19. SARS, MERS, influenza, Ebola, dengue, yellow fever, chikungunya, West Nile, Lassa, Japanese encephalitis, Epstein-Barr, and polio can all be deadly in one person but asymptomatic in the next.

    But for most of human existence, we didn’t know that viruses could infect us asymptomatically. We didn’t know how to look for them, or even that we should. The tools of modern science have slowly made the invisible visible: Antibody surveys that detect past infection, tests that find viral DNA or RNA even in asymptomatic people, and mathematical models all show that viruses are up to much more than making us sick. Scientists now think that for viruses, a wide range of disease severity is the norm rather than the exception.

    A virus, after all, does not necessarily wish its host ill. A dead host is a dead end. The viruses best adapted to humans have co-evolved over millions of years to infect but rarely sicken us. Human cytomegalovirus is a prime example, a virus so innocuous that it lives in obscurity despite infecting most of the world’s population. (Odds are that you have it.) Infections with human cytomegalovirus are almost always asymptomatic because it has evolved a suite of tricks to evade the human immune system, which nevertheless tries its best to hunt the virus down. By the time humans reach old age, up to a quarter of our killer T cells are devoted to fighting human cytomegalovirus. Pathogens and immune systems are in constant battle, with one just barely keeping the other in check. In the rare instances when human cytomegalovirus turns deadly—usually in an immunocompromised patient—it’s because this equilibrium did not hold.

    The coronavirus that causes COVID-19 is much newer to humans, and severe cases have justifiably gotten the most attention during the pandemic. Scientists have made dramatic advances in understanding this virus and how to treat it. But unraveling why it makes some of us sick, and leaves others unscathed, requires an appreciation of the delicate dance between pathogen and immune system that begins each time the virus finds a new host.

    Let’s begin where a COVID-19 infection begins, when virus meets cell. The initial infectious dose—the number of virus particles that enter the body—may influence the course of infection. The more particles that land in your nose, for example, the closer the virus is to overwhelming your immune system, leading in some cases to more severe illness.

    Within hours of a typical viral infection, the first infected cells begin secreting interferons, a group of molecules that acts as “a fire alarm and sprinkler system in one,” says Angela Rasmussen, a virologist at Georgetown’s Center for Global Health Science and Security. The fire alarm alerts the two main branches of the human immune system: the fast but nonspecific innate immune system, which causes inflammation and fever, and the adaptive immune system, which over a series of days will muster antibodies and T cells that more precisely target the invading virus.

    Interferons also “interfere” with the virus in a number of ways, such as degrading viral genes, preventing cells from taking up viral particles, suppressing the manufacturing of viral proteins, and causing infected cells to self-destruct. By slowing replication of the virus, interferons buy time for the rest of the immune system.

    This is what happens when everything goes right. But every successful virus has to develop ways of evading the body’s defenses, and the coronavirus that causes COVID-19 is very good at a devilish trick: Several of its genes encode proteins that seem capable of blocking interferons. By quieting the body’s fire alarm and disarming its sprinkler system, the coronavirus can set fire after fire. In the race between virus and immune system, the immune system falls behind. The virus proliferates. Lung cells die.

    Eventually, so many viral particles are infecting so many cells that the immune system knows something must be wrong. It begins to gear up—but too late. Without timely targeted strikes from the adaptive immune system’s antibodies and T cells, the powerful but blunt innate immune response ramps up and up, destroying healthy human cells in the process. This is one possible explanation for the immune overreaction observed in severe and fatal cases of COVID-19.

    This delayed interferon response, Rasmussen told me, reminds her of Ebola, which she studied before our current pandemic. Ebola is a very different virus with a much higher fatality rate, but deadly cases of Ebola are also characterized by uncontrolled inflammation in the body following a delayed interferon response. And Ebola is asymptomatic in some people too—as many as a quarter of all those infected, according to one estimate. Surveys in outbreak areas have found many people with antibodies against Ebola but no recollection of illness.

    Some of the differences among patients’ interferon responses might be genetic. When Dutch doctors investigated severe COVID-19 cases in two pairs of brothers, they found that all four had a genetic mutation that impaired interferon production. The brothers, who were from two different families, were all healthy and young, from 21 to 32 years old. One of them died of COVID-19, and all four needed to be put on ventilators in an intensive-care unit. But their specific mutation is not common, and genetics are unlikely to completely explain the variation in COVID-19 cases. Every scientist I spoke with emphasized how little we know. “It would be an understatement to say we do not fully understand,” Alessandro Sette, an immunologist at the La Jolla Institute, told me.

    The asymptomatic end of the severity spectrum is the most difficult to study. The first challenge is finding the cases: Asymptomatic people do not come to the hospital and are unlikely to get tested. If they are tested, their early immune response is typically long over by the time results come back. Finding asymptomatic patients usually means following a large group of healthy people for a long time, waiting for some of them to catch the virus of interest.

    In the summer of 2020, Antonio Bertoletti, a virologist at Duke-NUS Medical School in Singapore, had one such opportunity to study asymptomatic COVID-19 patients. Although Singapore had so far largely controlled the spread of COVID-19, an outbreak was raging among its migrant workers, many of whom were from India and Bangladesh. To contain the outbreak, the government paid the workers to isolate at home and track their symptoms with thermometers and oximeters. During the isolation period, Bertoletti and his colleagues recruited 478 workers who were willing to have their immune responses tracked through periodic blood samples. Over a six-week period, about a third of the study participants caught and recovered from COVID-19. A large majority of cases were asymptomatic, and the rest were mostly mild.

    Bertoletti and his colleagues were interested in virus-specific T cells that are essential to the adaptive-immune response. When they isolated these cells from blood samples, they found that asymptomatic patients had more specific and coordinated T-cell responses with high levels of an antiviral molecule and another that regulates other T cells. Their adaptive immunity looked more “fit,” Bertoletti told me. The sicker patients’ cells released a broader range of inflammatory molecules, suggesting that their immune response was less targeted.

    Although COVID-19 antibodies got a lot of attention early in the pandemic, T cells are now emerging as key to fighting COVID-19. Patients can recover from COVID-19 without antibodies at all—as long as they have T cells to fight the virus. T cells may play an additional role in milder infections: Depending on where in the world you look, some 28 to 50 percent of people have T cells that predate the pandemic but nevertheless react to the new virus. These T cells may be remnants of infections with related coronaviruses, a theory supported by one study, which found that people who were more recently infected by other coronaviruses tended to have milder COVID-19 infections. In Singapore, 93 percent of the cases Bertoletti found were asymptomatic—a much higher percentage than in other closed settings, such as cruise ships—a result he attributes to the migrant workers’ relative youth and possible cross-reactive T cells, which seem to be more common in some parts of the world than in others. To further understand the role of cross-reactive T cells, Sette, at La Jolla, is studying whether patients who possess them also mount a stronger immune response after receiving a COVID-19 vaccine.

    T cell responses also weaken with age, which may help explain why COVID-19 is dramatically more deadly for the elderly. Humans have a huge diversity of T cells, some of which are activated each time we encounter a pathogen. But as we age, our supply of unactivated T cells dwindles. Immunosenescence, or the gradual weakening of the immune system over time, is influenced by both age and the system’s previous battles. Human cytomegalovirus—that otherwise innocuous virus that infects much of the world’s population—seems to play a particular role in immunosenescence. So many of our T cells are devoted to suppressing this virus that we may become more vulnerable to new ones.

    Unlike human cytomegalovirus, the coronavirus doesn’t seem capable of hiding inside our bodies in the same way for decades. Once it sneaks in, its goal is to replicate as quickly as possible—so that it can find another body before it kills its host, or its host eliminates it.

    Now that this coronavirus has found humans, it will have a chance to hone its strategy, probing for more weaknesses in the human immune system. That doesn’t necessarily mean it will become more deadly the four coronaviruses already circulating among humans cause only common colds, and the virus that causes COVID-19 could one day behave similarly. Variants of the virus are already exhibiting mutations that make them more transmissible and better able to evade existing antibodies. As the virus continues to infect humans over the coming years, decades, and maybe even millenia, it will keep changing—and our immune systems will keep learning new ways to fight back. We’re at the very beginning of our relationship with this coronavirus.

    The Atlantic’s Covid-19 coverage is supported by a grant from the Chan Zuckerberg Initiative.

    How Do White Blood Cells Work?

    White blood cells are the body’s first line of defense against invaders, whether they're viral, bacterial, or parasitic. These cells include lymphocytes, which have slightly different functions depending on their structural makeup.   T cells, for example, are named for their ability to curb tumor growth, B cells have an ability to produce antibodies, and NK cells, or “natural killer” cells, are able to cause apoptosis, or cell death.

    Blumberg says that a low lymphocyte count is not necessarily a reflection of the quality of baseline immune system function.

    “It is possible that these immune cells provide primary protection against disease and control the infection,” Blumberg says. “However, an alternative explanation is that SARS-CoV-2 infection results in depression of the lymphocyte count in symptomatic patients who have a more invasive infection—we often see this with viral infections. So the difference in lymphocyte counts may be the result of severe infection, and might not indicate protection in those who are ultimately asymptomatic.”

    According to Blumberg, disparate factors can affect your lymphocyte count, including:

    • Age
    • Stress level
    • Medical history (including HIV infection, tumor development, and cancer treatment)

    Children, for example, tend to have a higher lymphocyte count than adults, which could explain why preteens and teenagers seem to be less susceptible to COVID-19 than older adults.  

    Signs and Symptoms of Disease

    An infection is the successful colonization of a host by a microorganism. Infections can lead to disease, which causes signs and symptoms resulting in a deviation from the normal structure or functioning of the host. Microorganisms that can cause disease are known as pathogens.

    The signs of disease are objective and measurable, and can be directly observed by a clinician. Vital signs, which are used to measure the body’s basic functions, include body temperature (normally 37 °C [98.6 °F]), heart rate (normally 60–100 beats per minute), breathing rate (normally 12–18 breaths per minute), and blood pressure (normally between 90/60 and 120/80 mm Hg). Changes in any of the body’s vital signs may be indicative of disease. For example, having a fever (a body temperature significantly higher than 37 °C or 98.6 °F) is a sign of disease because it can be measured.

    In addition to changes in vital signs, other observable conditions may be considered signs of disease. For example, the presence of antibodies in a patient’s serum (the liquid portion of blood that lacks clotting factors) can be observed and measured through blood tests and, therefore, can be considered a sign. However, it is important to note that the presence of antibodies is not always a sign of an active disease. Antibodies can remain in the body long after an infection has resolved also, they may develop in response to a pathogen that is in the body but not currently causing disease.

    Unlike signs, symptoms of disease are subjective. Symptoms are felt or experienced by the patient, but they cannot be clinically confirmed or objectively measured. Examples of symptoms include nausea, loss of appetite, and pain. Such symptoms are important to consider when diagnosing disease, but they are subject to memory bias and are difficult to measure precisely. Some clinicians attempt to quantify symptoms by asking patients to assign a numerical value to their symptoms. For example, the Wong-Baker Faces pain-rating scale asks patients to rate their pain on a scale of 0–10. An alternative method of quantifying pain is measuring skin conductance fluctuations. These fluctuations reflect sweating due to skin sympathetic nerve activity resulting from the stressor of pain. [1]

    A specific group of signs and symptoms characteristic of a particular disease is called a syndrome. Many syndromes are named using a nomenclature based on signs and symptoms or the location of the disease. Table 1 lists some of the prefixes and suffixes commonly used in naming syndromes.

    Table 1. Nomenclature of Symptoms
    Affix Meaning Example
    cyto- cell cytopenia: reduction in the number of blood cells
    hepat- of the liver hepatitis: inflammation of the liver
    -pathy disease neuropathy: a disease affecting nerves
    -emia of the blood bacteremia: presence of bacteria in blood
    -itis inflammation colitis: inflammation of the colon
    -lysis destruction hemolysis: destruction of red blood cells
    -oma tumor lymphoma: cancer of the lymphatic system
    -osis diseased or abnormal condition leukocytosis: abnormally high number of white blood cells
    -derma of the skin keratoderma: a thickening of the skin

    Clinicians must rely on signs and on asking questions about symptoms, medical history, and the patient’s recent activities to identify a particular disease and the potential causative agent. Diagnosis is complicated by the fact that different microorganisms can cause similar signs and symptoms in a patient. For example, an individual presenting with symptoms of diarrhea may have been infected by one of a wide variety of pathogenic microorganisms. Bacterial pathogens associated with diarrheal disease include Vibrio cholerae, Listeria monocytogenes, Campylobacter jejuni, and enteropathogenic Escherichia coli (EPEC). Viral pathogens associated with diarrheal disease include norovirus and rotavirus. Parasitic pathogens associated with diarrhea include Giardia lamblia and Cryptosporidium parvum. Likewise, fever is indicative of many types of infection, from the common cold to the deadly Ebola hemorrhagic fever.

    Finally, some diseases may be asymptomatic or subclinical, meaning they do not present any noticeable signs or symptoms. For example, most individual infected with herpes simplex virus remain asymptomatic and are unaware that they have been infected.

    Think about It

    Examples of Noninfectious Diseases

    Several examples of noninfectious diseases are described below. The diseases represent a diversity of types of diseases, ranging from purely genetic to primarily environmental diseases.

    Cystic Fibrosis

    Cystic fibrosis is an example of a genetic noninfectious disease. It is caused by an inherited mutation in a gene called CFTR. Mutant versions of the gene produce a faulty protein that normally helps to move sodium chloride into and out of cells. The impaired salt transfer causes mucus to be abnormally thick and sticky. Figure (PageIndex<3>) helps explain the diversity of negative health impacts that may occur in people with cystic fibrosis. The thick mucus accumulates in the organs of the airways. This may lead to resurrect respiratory and sinus infections. This may also lead to malabsorption. The mucus blocks passages in mucus-secreting organs such as the lungs, pancreas, reproductive system, and intestine.

    Figure (PageIndex<3>): This figure explains how a single defective gene resulting in thick mucus can lead to severe health problems body-wide.

    There is no known cure for cystic fibrosis, but recent advances in the treatment of cystic fibrosis allow people with the disease to live healthier and longer lives. A few generations ago, a newborn with cystic fibrosis was unlikely to live beyond the first year of life. Today, people with cystic fibrosis are likely to live to middle adulthood. Lung infections and other lung problems cause the greatest disability and premature death in people with cystic fibrosis. Therefore, treatment usually includes the proactive use of antibiotics and other drugs to fight off infections, along with pulmonary rehabilitation to maximize lung function. Even with treatment, however, lung damage may eventually progress to the point where a lung transplant is needed.

    The mutant CFTR gene for cystic fibrosis is a recessive gene located on an autosome (chromosome 7). As with any autosomal recessive trait, an individual must have two copies of the mutant gene to develop the disease. An individual with just one copy of the normal CFTR gene can produce enough of the functioning protein to secrete normal mucus and avoid the signs and symptoms of cystic fibrosis. Such a person is called a carrier of cystic fibrosis. Carriers can pass the mutant gene to their offspring. The inheritance pattern of an autosomal recessive disease such as cystic fibrosis is shown in the pedigree diagram in Figure (PageIndex<4>).

    Without medical intervention, cystic fibrosis is fatal in infancy, yet the mutant gene that causes it has been maintained at relatively high levels in some human populations for tens of thousands of years. The mutant gene is most common in people of Northern European ancestry. In these populations, about 1 in 25 people is a carrier, and about 1 in 3,000 newborns have cystic fibrosis. The most common explanation for the persistence of the cystic fibrosis mutation is some type of heterozygote advantage in carriers of the mutant gene. For example, it has been hypothesized that carriers of the cystic fibrosis mutation may have greater-than-normal resistance to certain infectious diseases, such as cholera, typhoid fever, or tuberculosis.

    Figure (PageIndex<4>): This pedigree shows that people affected by an autosomal recessive disease such as cystic fibrosis must have two carrier parents. The image shows two carrier parents. According to the Punnett square, the probability of them having a normal child is 75%, and the probability of them having a child with cystic fibrosis is 25%. Twenty five percent of the normal children will be non carrier and fifty percent will carry the gene without any symptoms of the disease.


    Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. Cancer is one of the top ten causes of death in high-income countries. Most cancers are diagnosed in people over the age of 65 only a few types of cancer occur in children. It is likely that if one were to live long enough and avoid other common causes of death, such as cardiovascular diseases and diabetes, sooner or later a person would succumb to cancer.

    About 90 percent of cancers are noninfectious diseases. (About 10 percent of cancers are infectious diseases caused by pathogens, such as the human papillomavirus, which causes cervical cancer.) Rather than pathogens, noninfectious cancers are caused by some combination of genetic and environmental factors. About 10 percent of cancers are caused largely by genes or have a very strong genetic influence. For example, inheriting genes called BRCA1 and BRCA2 increase the risk of women developing breast or ovarian cancer by as much as 75 percent.

    Most cancers are caused largely by environmental factors, including human behaviors. For example, tobacco smoke contains 50 known carcinogens or cancer-causing agents, and smoking causes 90 percent of lung cancers. You can see the connection between smoking and lung cancer in Figure (PageIndex<5>). Like most such environmental factors and cancer, it generally takes many years of exposure to tobacco smoke before lung cancer develops. Lung cancer is not the only kind of cancer caused by tobacco use. Smoking also increases the risk of cancer of the larynx, head, neck, stomach, bladder, kidney, esophagus, and pancreas.

    Figure (PageIndex<5>): Based on data from the mid-1900s, this graph shows that the more cigarettes men smoked, the greater was their risk of dying from lung cancer. It also shows that smokers generally died from lung cancer about two decades after they began smoking.

    Other behaviors that play major roles in causing cancer include poor diet and physical inactivity, both of which contribute to high rates of obesity. These factors are responsible for at least a third of cancer deaths. Additional environmental causes of cancer include the radioactive gas radon from underground rocks and ultraviolet radiation from the sun. Radon increases lung cancer risk, and UV radiation is the primary cause of skin cancer.

    Many treatment options exist for cancer. The primary treatments include surgery, chemotherapy, and radiation therapy. Which treatments are used depends on factors such as the type and location of cancer and whether cancer has spread. Treatments may or may not be curative. You can learn more about cancer by reading the concept of Cancer.

    Cardiovascular Disease

    Cardiovascular disease refers to a class of diseases that involve the heart or blood vessels. The diseases include coronary artery disease, stroke, and peripheral artery disease. (You can read more about specific types of cardiovascular disease in the concept of Cardiovascular Disease.) Cardiovascular disease is the leading cause of death worldwide, with about 30 percent of deaths attributable mainly to cardiovascular disease. By the year 2030, an estimated 23 million people a year will die from cardiovascular disease.

    Two major precursors of cardiovascular disease are hypertension and atherosclerosis.

    • Hypertension is defined as blood pressure that is persistently elevated. Controlling hypertension either through medications or lifestyle changes is important for reducing the risk of all types of cardiovascular diseases, but especially stroke.
    • Atherosclerosis is a condition in which artery walls thicken and stiffen as a result of the buildup of fatty plaques inside the arteries (Figure (PageIndex<6>)). The buildup of plaques in arteries actually starts in childhood and continues in most people throughout life. The progression of atherosclerosis can be controlled through lifestyle approaches, including eating a healthy diet, getting regular exercise, and avoiding tobacco smoke. Medications to lower blood triglycerides and raise HDL levels may also help.

    Obesity and diabetes are additional major risk factors for cardiovascular disease. Obesity is associated with other risk factors for cardiovascular disease, including hypertension and high blood triglycerides, but it may also have an independent effect on cardiovascular disease risk. People with diabetes are two to four times more likely than nondiabetics to die of cardiovascular disease.

    Most cases of cardiovascular disease could be prevented by modifying risk factors. Some risk factors, such as hypertension and high blood triglycerides, can be controlled with medications. Other risk factors, such as obesity and physical inactivity, can be controlled by adopting healthy behaviors (such behaviors may also help control hypertension and high blood lipids even without medications). Although modifiable environmental factors such as these are the main risk factors for cardiovascular disease, genes also play an important role. A person&rsquos risk of developing cardiovascular disease is three times greater than the average if the person&rsquos parents had cardiovascular disease. However, age is by far the most important risk factor for diseases of the heart or arteries. There is a tripling of cardiovascular disease risk with each passing decade of life.

    Type 2 Diabetes

    Diabetes is diagnosed in people who have abnormally high levels of blood glucose over prolonged periods of time. Symptoms of untreated high blood glucose include frequent urination, increased thirst, and increased hunger. As of 2016, an estimated 422 million people worldwide had diabetes, with the rates being somewhat higher in developed countries.

    There are several types of diabetes, but type 2 diabetes is by far the most common. It accounts for about 90 percent of all cases of diabetes. Type 2 diabetes generally develops due to insulin resistance, rather than lack of insulin, which occurs in type 1 diabetes. As illustrated in Figure (PageIndex<7>), insulin resistance occurs when cells of the body become increasingly unresponsive to insulin due to malfunctioning insulin-receptor sites. Cells can no longer take up enough glucose from the blood to maintain glucose homeostasis. In many cases of type 2 diabetes, the problem of insulin resistance is exacerbated by a secondary reduction in insulin secretion.

    Figure (PageIndex<7>): The mechanism that underlies most type 2 diabetes is insulin resistance, which leads to elevated levels of glucose in the blood. On the left, it shows two receptors piercing through the plasma membrane of a cell. The blue ball represents insulin which is attached to its receptor. This attachment is necessary for the glucose channels to open. The glucose is flowing into the cell through open glucose channels. On the right, you see the same types of receptors. Insulin is attached to its receptor, but it is not causing the glucose channels to open. This leads to the accumulation of glucose in the blood.

    Type 2 diabetes typically starts after the age of 40. It is most likely to be diagnosed in people who are obese and have other indicators of metabolic syndrome, which is sometimes referred to as pre-diabetes for this reason. Because of the dramatic increase in recent decades in obesity in younger people, the age at which type 2 diabetes is diagnosed has fallen. Even children are now being diagnosed with type 2 diabetes. Today, about 30 million Americans have type 2 diabetes, and another 90 million Americans have pre-diabetes.

    Unless diabetes is carefully monitored and controlled, high blood sugar levels can eventually lead to heart attacks, strokes, blindness, kidney failure, and many other serious health problems. These complications of diabetes are primarily due to damage to small blood vessels caused by inadequately controlled blood glucose levels. All else being equal, the risk of death in adults with diabetes is 50 percent greater than it is in adults without diabetes.

    Controlling type 2 diabetes usually requires frequent blood glucose testing, watching what and when you eat and taking oral medications or even insulin injections. Changing your lifestyle may stop the progression of type 2 diabetes or even reverse it. By adopting healthier behaviors, you may be able to keep your blood glucose level within the normal range without medications or insulin.

    Watch the video: Ζυγούλη: Έχω επιλέξει να είμαι κοντά στα παιδιά - Ο Σάκης θέλει συνεχώς να μαθαίνει νέα πράγματα (July 2022).


  1. Shepherd

    What do you advise me?

  2. Garadin

    In all this the matter.

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