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Covid-19, why is it that people manifest such differences in their response to infection? Why is it so impossible (at least at present) to predict an individual’s experience?

The consequences as we have seen and read about of being diagnosed with Covid-19 appears to come with a wide range of risks and symptom intensity.

To understand this complex question, we need to get our terminology right. “Infection” means acquisition of the coronavirus after exposure to it. Infection is not synonymous with exposure — or with disease.

“Disease” is a clinical state associated with cough, fever and other symptoms that ranges from mild to severe. These symptoms arise from damage to tissues and the immune system. Death occurs when there is so much damage that the body cannot maintain blood oxygenation and other vital functions.

Historically when epidemics were in action, death and survival were attributed to a variety of explanations including providence or fortune. Today, medicine and science provide a better understanding of why infection can lead to such different outcomes. Among individuals in the same risk group — the same age, say — differences in infection outcome can result from various variables with some within and others outside their control.

  1. Inoculum: the number of viral particles that cause infection. Essentially smaller numbers of viral particles are more likely to be contained effectively by the body’s defences. Then, infection may cause no symptoms or only mild disease. In contrast, many particles can lead to increased viral growth, overwhelming the immune system and causing more severe disease. This reflects a variable exposure response curve, depending on the viability of the individual’s immune capability and response.
  2. Genetics: A germ lined encoded susceptibility to severe infection response may exist. Viruses will gain access to host cells via surface proteins, which vary in number and nature between individuals. Someone with no such surface proteins may be resistant to infection. In the case of HIV, for example, some people lack the receptors needed for viral infection and are not susceptible to the virus, think current focus on ACE2 receptors amongst others. Plus of course how lifestyle choices and medications impact all gene encoded receptors and gene expression, including those involved in immune responses.
  3. Route of Infection: Infection outcome is influenced by the route of viral entry. Aerosolised inhalation may determine a different outcome to hand transfer to mucous membranes. Nose and lung have different response capabilities. It is possible that a virus inhaled in the form of aerosolised droplets, triggers different immune defences than does a virus acquired by touching contaminated surfaces and then touching one’s face. The nose and the lung differ in local defences, so the route of infection could significantly affect the outcome.
  4. Strength of the coronavirus itself. Viruses differ in virulence — their capacity to damage host tissues or impact immune responses — even when they are all the same species. Hence why flu seasons vary in severity from year to year. The varieties of a virus such as coronavirus differ depending on small genetic characteristics and how these affect the interaction with human hosts. As the coronavirus spreads from person to person, it may undergo unique changes in its genetic structure that enhance or attenuate its capacity to do harm. Strains that are more virulent could lead to more severe disease.
  5. People’s immune status — Current and prior infectious experiences will determine response to infection. The immune system remembers previous encounters with microbes, and that affects how it fights and responds to new ones. A recent infection with a virus can affect susceptibility to an unrelated new infection. For example, having had the flu before a coronavirus infection, could change the course of the Covid-19 disease in unpredictable ways. When a person’s immune system has no memory of an infectious agent, it may be unable to rapidly respond, and this may allow the invader to escape detection, giving it more time to cause damage. This can affect the ability to generate anti-inflammatory cytokines, neutralising antibodies, Tcells and mucosal barrier competence and sIgA production etc.
  6. Peoples exposome exposure: Genetic expressions are strongly mediated by the environmental contexts within which biological materials manifest and operate. What perfuses our environment can thus shape and become biology. Toxic effects are mediated through chemicals that alter critical molecules, cells, and physiological processes inside the body including the immune system. Under this view, exposures are not restricted to chemicals (toxicants) entering the body from air, water, or food, for example, but also include chemicals produced by inflammation, oxidative stress, lipid peroxidation, infections, gut flora, and other natural processes, all of which are mediated by food and lifestyle choices or experiences.
  7. People’s current health status. Body mass, age, gender, residence, comorbid conditions (asthma, chronic lung disease, heart conditions, kidney disease, immunocompromised, liver disease, cancer etc.), and state of fitness all contribute to relative risk. Males over 65 with a pre-existing co morbidity and fitting the definition of being obese are the highest risk category for hospital admission and death.
  8. People’s nutrition and wellbeing status: The human immune system is intimately dependent on the bioavailability of nutrients either extracted from foods, or by ingestion of concentrated forms. Deficiency in key nutrients such as vitamin D, A, C, and the minerals zinc and selenium are known to impair immune responses to viral infections. Stress, sleep and living conditions also impact the immune systems capacity to respond and will influence symptoms and recovery.

Taken together, these variables create a complex picture and combine to produce outcomes ranging from asymptomatic infection to death. And because these parameters can vary so much from infected person to infected person, it’s impossible to predict the related symptom profile and ultimate outcome. Therefore, despite accumulating evidence that most who acquire the coronavirus will not develop severe disease, the uncertainty of who is at grave risk enhances the pandemic’s related anxiety.

However, its clear that only a small percentage of infected people need acute hospital care, and we have a personal and social responsibility to contribute to risk reduction, this article in Medium summarises some of the current best practices. The American Nutrition Association have a regularly updated source of science backed summaries on the role of nutrition and The Journal of Medical Virology posted a systematic review looking at nutrition and Covid-19.

5 responses to “COVID-19 What must happen to become infected”

  1. Donna says:

    Please could you give an explanation as to the mooted increased risk of developing this disease if you have had the standard winter flu vaccine.

    Also, if you have had asthma in the past but through diet and lifestyle changes have managed to be symptom-free for a few years…. are you still at higher risk?

  2. Elizabeth Downing says:

    Excellent. Thank you, this will be used with my clients.

  3. Roz Kadir says:

    What’s your opinion on salt pipes with iodine as Dr Myhill suggests?

  4. Michael Ash says:

    There has been a somewhat overreached discussion concerning the question does a flu vaccination add additional risk to someone who subsequently becomes infected with SARS-Cov-2, namely that the flu shot has been shown to cause a 36% increase in coV-2 infections, here are links to the original article, which is being sited to support this claim, and two links to a popular and a scientific rebuttal.

    The original article used by people to try and “prove” that the flu shot leads to a 36% increase in coronavirus infections:
    https://pubmed.ncbi.nlm.nih.gov/31607599/

    This is an easier to understand rebuttal of this claim:
    https://www.usatoday.com/…/fact-check-flu…/2933900001/

    A more scientific response to the claim:
    https://healthfeedback.org/…/claim-that-flu-vaccine…/

    There are many early call outs on various proposals, its quite typical that in the time period where much more is not known, than is known that gaps in knowledge permit different interpretations than may eventually be found to be more consistent. i.e the recent expectation that Gileads medicine would be effective, and quite possibly that Hydroxychloroquine will be less effective than hoped, or more? Its into these gaps that uncertainty, pushed with a burst of the individual need to be validated can lead to unsupported memes gaining traction. At this stage, the position is that prior vaccination does not make you likely to overreact. But by the same vein, despite people with a respiratory disease caused by smoking having a far higher risk of death than non-smokers, a French study has tentatively suggested some people may be protected by smoking – early days, and many variables to follow yet!

    In terms of a prior but lifestyle resolved asthma, you might reasonably conclude that the overall benefits of the changes that altered your asthma are also likely to have improved other health related parameters. If the resolution and associated intervention have been ongoing for some time, it’s probable that your risk factors now align with similarly healthy people with no history of respiratory sensitivity.

  5. Michael Ash says:

    There is no clear evidence of its role in Coronavirus (related family of) efficacy we know of, but the basic mechanisms have applicability, and if done correctly has low risk.

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