Coronavirus – the importance of our immune response
As the UK government starts to plan how the country will move out of lockdown and “back to work”, many of us are still unsure about leaving the house, unsure how will testing help and whether or not we will be tested, some of us are still shielding or just simply concerned about the increased possibility of infection post lockdown, especially in densely populated city areas.
We consider in this article the multi-faceted factors of coronavirus, and what predicates our potential for contracting COVID-19. Why is it that people manifest such differences in their response to infection? Why does it seem impossible to predict an individual’s experience?
Predicting the response
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 variables, some within, and others outside their control.
- 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. The 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.
- 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. Lifestyle choices and medications impact all gene-encoded receptors and gene expression, including those involved in immune responses.
- 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 aerosolized 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.
- 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 a 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.
- 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, T-cells and mucosal barrier competence and sIgA production etc.
- 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 the 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.
- 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 comorbidity and fitting the definition of being obese are the highest risk category for hospital admission and death.
- 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 A, C, D and the minerals zinc and selenium are known to impair immune responses to viral infections. Stress, sleep and living conditions also impact the capacity of the immune system 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, but there are aspects that we individually can take steps to control and influence and perhaps improve our immune systems, even in the face of our modern living environments.
The impact of chronic conditions on the immune response
Across the pond, an article from The Hill points to the prevalence of underlying chronic conditions and the strong correlation to COVID-19 mortality. For example, obesity is a key risk factor for COVID-19 hospitalisations in New York City. It goes onto say that our immune response to a virus is very much impaired by a combination of processed food and poor living choices, nudging our health status ever downwards. Food, farming and pharma industries supported by government policies ultimately weaken our societal immunological capability to respond to a virus pandemic, concluding that:
Americans must build personal immunity defences through radical changes in diet and exercise, or risk getting sick and dying.
In an Atlantic article, “Why some people get sicker than others” they consider the impacts of wider social-economic inequality, the outputs of which (e.g. poorer food choice opportunities and poor air quality) result commonly in weakened individual immune responses. Thus creating a vulnerable society ripe for a poor outcome from a viral pandemic.
Variation in immune responses between people is due to much more than age or chronic disease. The immune system is a function of the communities that brought us up and the environments with which we interact every day. Its foundation is laid by genetics and early-life exposure to the world around us — from the food we eat to the air we breathe. Its response varies on the basis of income, housing, jobs, and access to health care…Ultimately, people who are unable to take time off of work when sick — or who don’t have a comfortable and quiet home, or who lack access to good food and clean air — are likely to bear the burden of severe disease.
Stress levels, sleep, food and exercise are all significant factors for improving your immune system and importantly, we have control over these areas of our lives, so with the current pandemic, the expected easing of lockdown and our future individual health it would make sense for all of us to optimise our immune capability where we can.