As the pandemic of COVID-19 progresses we are learning more about the virus. In asymptomatic cases, the role of humoral immunity is unclear. Are antibodies elicited from asymptomatic cases? If so, how long do they last? To answer such questions, a team of researchers compared antibody responses in 405 asymptomatic individuals with 459 symptomatic COVID-19 patients. They found that IgM responses rapidly declined in both groups.
However, they found striking differences concerning the strength and persistence of SARS-CoV-2-specific IgG responses. The team has released their results on a preprint server. The IgG responses (both prevalence and durability) and neutralizing capacities correlated positively with the COVID-19 symptoms. Particularly, those antibodies recognizing the RBD (receptor-binding domain) of the S (Spike) protein of SARS-CoV-2, which comprise neutralizing IgG molecules.
The researchers noted that regardless of sex, age, and body weight, asymptomatic individuals lost their SARS-CoV-2-specific IgG antibodies more often and rapidly than symptomatic patients. The results suggest that a considerable fraction of asymptomatic natural infections stimulate a humoral immune response conferring the ability to resist reinfections. The findings are important for understanding the immunity against SARS-CoV-2 and for designing immunization programs including individuals after asymptomatic infections.
The researchers tested the plasma levels of immunoglobulin G (IgG) and M (IgM) against the viral spike or nucleoprotein. The researchers also observed that the duration of viral RNA shedding seems to be shorter in asymptomatic cases.
A shorter virus replication phase may be associated with an antigen availability that is simply not long enough to prime optimal B-cell and/or antibody responses. The researchers also discussed other possible explanations for early symptoms and strong, long-lasting IgG responses: 1) the association between innate immune responses and symptoms, as opposed to innate immune responses and antibody responses; and 2) the overlapping dependence on interferons, which enhance antibody responses and induce class switching.