Self-isolation may increase susceptibility to Covid-19: Study
Researchers now claim that time spent in isolation may actually increase the vulnerability to upper respiratory viruses and perhaps coronavirus (Covid-19).
“We know little about why some of the people exposed to the coronavirus that causes Covid-19, are more likely to develop the disease than others,” said study author Sheldon Cohen from the Carnegie Mellon University in the US.
“However, our research on psychological factors that predict susceptibility to other respiratory viruses may provide clues to help identify factors that matter for Covid-19,” Cohen added.
Through a series of viral challenge studies, the researcher examined how such factors can affect whether or not healthy adults exposed to respiratory viruses become ill.
Cohen work has focused on eight viral strains that cause common cold and two that cause influenza.
“In our work, we intentionally exposed people to cold and influenza viruses and studied whether psychological and social factors predict how effective the immune system is in suppressing infection, or preventing or mitigating the severity of illness,” he said
To slow the spread of coronavirus, many communities issued stay-at-home measures, increasing interpersonal stressors, like loneliness, loss of employment and familial conflict.
According to Cohen, these stressors may be powerful predictors of how a person will respond if exposed to coronavirus.
In a series of studies, he found participants experiencing interpersonal stressors had a greater chance of developing upper respiratory illnesses when exposed to cold viruses.
Cohen believes interpersonal stressors might play a similar role in response to the coronavirus causing Covid-19, increasing a person’s vulnerability to infection and illness.
In addition, both social and psychological stressors increased the production of cytokines, molecules that promote inflammation in response to infection.
In Cohen’s work, psychological and social stressors were associated with an overproduction of pro-inflammatory cytokines in response to cold and influenza viruses. In turn, this excess of inflammation was associated with an increased risk of becoming ill.
Similarly, research on Covid-19 has shown that producing an excess of pro-inflammatory cytokines is associated with more severe Covid-19 infections suggesting the hypothesis that a stress-triggered excessive cytokine response might similarly contribute to excessive inflammation and symptoms in Covid-19.
Cohen’s work has pointed to the importance of social and psychological factors in the development of infection and illness. This work may hold clues to the health implications of the on-going quarantine.