By Pooja Tripathi
The news pieces on coronavirus are replete with instances of a 90-year-old being treated and one in 20s succumbing to the infection. As seen in every story of an epidemic, some die, some become carriers, some recover, and the luckiest live through infection giving further insight to science. This is exactly what, we are seeing in front of our eyes.
Although the initial epidemiological data showed that Covid-19 is more severe in immunocompromised people, men and those with pre-existing conditions such as heart and lung disease. It is important to know that not everyone with severe disease has these risk factors and not everyone at risk has the same symptoms, prognosis or outcome.
Why does the novel coronavirus manifest such differences? And why is it not possible to predict an individual’s experience? Let’s take you through some terms around infectious diseases.
Infection- The invasion and multiplication of microorganisms such as bacteria, viruses, and parasites that are not normally present within the body. An infection may cause no symptoms and be subclinical, or it may cause symptoms and be clinically apparent. An infection may remain localized, or it may spread through the blood or lymphatic vessels to become systemic. Disease is Illness or sickness characterized by specific signs and symptoms.
What is it that leads to infection progressing onto disease and then to death? As the massive, wearisome effort to stop the novel coronavirus pandemic presses on, it’s worth pausing to remember the successful eradication of another highly infectious and deadly virus: smallpox. The means of the smallpox eradication that involved understanding the viral load, meticulous surveillance, careful contact tracing, targeted vaccinations, and international cooperation—are worth remembering. They are precisely the tools that need to be sharpened and used to end the COVID-19 pandemic.
Talking about viral load, the knowledge about viral load is crucial as it could change the way we isolate, treat, and manage patients. The most important factor is microbial dose or inoculum, the number of viral particles that cause the infection. Small 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, a large number of particles can lead to increased viral growth, overwhelming the immune system and causing more severe disease.
What is the dose threshold for infection? That is, can we quantify the increase in the risk of infection as people are exposed to higher doses of the virus? Also, going by the novel nature of virus, does there exist a relationship between that initial “dose” of virus and the severity of the disease and the extent to which they are infectious to others during their peak. So far, in the early phases of the covid-19 pandemic, we have been measuring the spread of the virus across people. As the pace of the pandemic escalates, we also need to start measuring the virus within people.
There’s another aspect of transmission and disease: the host immune response. Viral attack and the immune system’s defense are two opposing forces, constantly at odds. Genetics may influence susceptibility to severe infection. Viruses often gain access to host cells via surface proteins, which vary in presence and nature from person to person.
HIV Infection and AIDS progression can throw some light into it. Once a person if infected with HIV, the virus count in the blood would rise to a tipping point, known as peak viremia and patients with the highest peak viremia typically started feeling sick sooner and developed fast progressing AIDS. More than peak viremia, what presented a better picture was set point—the level at which someone’s virus count settled after initial peak countering infection. This was a balance between the virus and host where they entered into a symbiotic relationship. People with a high set point tended to progress more rapidly to aids and people with a low set point frequently proved to be “slow progressors.” The viral load—a continuum, not a binary value—helped predict the nature, course, and transmissibility of the disease.
We have still not been able to differentiate the responsiveness based on route of infection. It’s possible that virus inhaled in the form of aerosols triggers different immune defences than does 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.
While studying viral load it may be important to also take into consideration the virulence of virus itself. Viruses differ in virulence — their capacity to damage host tissues or immunity — even when they are all the same species. A virus that is virulent in one setting may be innocuous in another, and a host may be susceptible or resistant depending upon age, route of infection, or properties of the virus. 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.
Quantifying viral loads may not only drastically change the treatment pattern but also will give us a fair idea of the prognosis. The quantitative approach of measuring viral load and corelating it to susceptibility can be applied to clinical drug trials as well as vaccine development. Clinical drug trials are typically more informative when run on subjects who are infected but are yet not critical; any therapy trial at the stage of ventilator in COVID-19 might be too little, too late. If the disease course in such patients is followed using viral-load metrics, rather than by tracking symptoms alone, the effect of a drug in different trials can be compared more easily and accurately.
A pandemic often comes with panic. Tracking an individual rather than containing the spread in a community would seem to be too indulgent and waste of resources. It is a prevention to control the bigger damage. This crisis requires that we measure and assess both the amount of risk as well as in intensity of risk hand in hand with the cure and control. That is the way to save lives from a disease as infectious as this.