The discussion – and disquiet amongst laypersons following news of the pandemic – intensified when a yet-to-be peer-reviewed study, published in medRxiv last week, assessed 90 recovered COVID-19 patients in the UK and found their nAbs decreased between two fold and 23-fold during an 18-65 day follow-up period.
Recent studies suggest that those recovering from COVID-19 may have antibodies for only a few months, a signal that long-term immunity is difficult to achieve, but several scientists dispel the gloom and say it is too soon to determine if such individuals can contract the disease again.
Some special cells of the immune system may still offer protection against the disease, the scientists said as questions swirl on whether people who have recovered from COVID-19 can get it again -- even those whose antibodies dwindle progressively as the days and weeks pass.
It is too soon to say whether people with lowered levels of novel coronavirus-blocking antibody levels (nAbs) after recovery are at risk of contracting the COVID-19 disease on re-exposure to the virus, Vineeta Bal, an immunologist from the Indian Institute of Science, Education and Research in Pune, told PTI.
"This pandemic is only six-seven months old, and reports of people testing positive for the virus for a second time, post-recovery, are mostly only from those who were first infected in January," Bal said in a video interview.
The discussion – and disquiet amongst laypersons following news of the pandemic – intensified when a yet-to-be peer-reviewed study, published in medRxiv last week, assessed 90 recovered COVID-19 patients in the UK and found their nAbs decreased between two fold and 23-fold during an 18-65 day follow-up period.
Another study, published last month in the journal Nature Medicine, surveyed the levels of antibodies in COVID-19 patients, including those who did not show symptoms, and revealed that nAbs lasted only two to three months after recovery.
While reports of people testing positive for re-exposure to the virus emerge, it does not necessarily mean that those losing nAbs will develop the disease, said Bal, who was a member of the Prime Minister's task force for women in science under the Ministry of Science and Technology.
It might take a year to get sufficient data to confirm this.
While antibody levels, as indicated by the two studies, may decrease in recovered individuals, other immune system players may still offer longer lasting immunity.
"Some reports say detectable T cells which may fight off infection and prevent the COVID-19 disease on re-exposure, can offer protection," Bal said.
Commenting on the implications of the studies, immunologist Satyajit Rath from the National Institute of Immunology in New Delhi, said the findings are in line with how the human immune system interacts with coronaviruses such as those causing the common cold.
In Rath's opinion, just like in other coronavirus infections, the more severe the COVID-19 disease, the higher the peak antibody levels' in patients as well as the tendency of their nAb levels to go down in weeks-to-months.
Asymptomatic infected individuals make very little nAbs to begin with, and may both recover and be protected by non-antibody-based mechanisms, he explained in an email interview.
"There is also some evidence that virus-specific T cells are activated and expanded in infected people, and they too can plausibly provide accelerated recovery re-infection," Rath said, adding a
caveat that there is no direct evidence for such an actual causal relationship.
According to the immunologist, if antibodies do play a major role, the two studies could mean that long term immunity both individually, and for the population, may be difficult to achieve.
Under such a scenario, he said, people may periodically keep getting re-infected and the "virus may keep spreading around" until effective vaccines come into widespread use.
There is no good evidence yet about this, and it may or may not be the case, he said.
Another study, published in the journal Nature on Wednesday, also revealed the involvement of T cells.
The research, conducted by scientists from the Duke-Nus Medical School in Singapore, found that individuals infected with SARS-CoV-2, or the 2002-03 SARS pandemic virus, or other coronaviruses,
develop memory T cells.
These coronavirus-specific T cells could last in the body for over 15 years after people recover from infection, and can still proliferate once they encounter a protein from that virus.
According to this study, patients who had recovered from the 2002-03 SARS virus 17 years ago still possess virus-specific memory T cells which cross-reacted with the current pandemic virus.
However, whether such pre-existing T cells affect the clinical manifestation of COVID-19 remains to be studied, said Nina Le Bert, a co-author of this study.
"However, if an individual already has memory T cells which recognise the new infection, the adaptive immune response could start earlier and may reduce the severity of COVID-19," she told PTI over email, wanting for more studies to confirm this.
According to Le Bert, the immune system is complex, and the different cell types usually complement each other.
"I believe that both cellular and antibody immunity will be equally important," she added.
Discussing the implications of the involvement of T cells in vaccine development, Bal said, "For a vaccine to be effective, it needs to generate reasonable concentration of nAbs and cytotoxic T cells."
"Then they can kill viruses on re-exposure," she said, adding that the combination makes "two components of a perfect vaccine".
She cautioned that vaccines which rely more on cell mediated immunity may not be effective in every individual to the same extent, compared to those which boost an antibody response alone.
Bal explained that this is due to genetic diversity of the global human population.
"Human cells have surface proteins called HLA antigens which are different for every individual. So there is no way to trigger a cell mediated immune response in a universal vaccine that is generalisable to everyone," she said.