PLoS Pathogens | 2021
Individuals cannot rely on COVID-19 herd immunity: Durable immunity to viral disease is limited to viruses with obligate viremic spread
Abstract
It is often messaged that herd immunity to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2 (CoV-2)), the causative agent of Coronavirus Disease 2019 (COVID-19), will protect nonvaccinated individuals from infection. Herd immunity refers to the concept that when a sufficient fraction of individuals in a population develop immunity from infection or vaccination, viral transmission is reduced to a near negligible level. However, seasonal CoVs, which cause approximately 20% of common colds, remain endemic, even though demonstrating only limited antigenic evolution in epitopes targeted by neutralizing antibodies [1,2]. Although there are only 4 circulating seasonal CoVs, infections frequently recur, even yearly, likely related to waning antibody levels [3]. Human challenge studies established that seasonal CoV reinfection with the identical strain can occur within a year after initial exposure, though typically with reduced shedding and milder symptoms [4]. Reinfection also appears to occur following mild COVID-19 cases, where the serum neutralizing antibody half-life is only approximately 5 weeks [5]. If immunity to SARS-CoV-2 and seasonal CoVs are similar, COVID-19 herd immunity is a pipe dream, even more so given the relatively rapid selection of mutants with amino acid substitutions in the spike protein that reduce the efficiency of serum antibody neutralization [6]. Absent effective herd immunity, over the next few years, individuals can choose whether their first exposure to SARS-CoV-2 immunogens occurs via vaccination or infection. With the agerelated increase in COVID 19 severity, it is critical that individuals be vaccinated sooner rather than later. Coronaviruses are hardly unique in their ability to reinfect humans. Infection with none of the common endemic human respiratory viruses consistently induces durable immunity (Table 1). Although influenza A and B viruses are notorious in this regard, they are, in a sense, less adept than the other respiratory viruses, which reinfect individuals without resorting to significant antigenic variation. Similarly, many viruses that infect the gastrointestinal (GI) tract can infect vaccinated or previously infected individuals, most likely due to waning immunity (Table 1). Unlike respiratory viruses, however, several GI viruses are well controlled by infection or vaccination, including poliovirus, now on the brink of vaccine-induced extinction. Poliovirus vaccination provides insight into the nature of protective antiviral immunity. Intramuscular immunization with inactivated virus prevents paralytic disease but not GI infection, with repeat vaccination necessary to reduce shedding of infectious virus. Similarly, even