Ultimately, our aim has been to pull together and appraise the current state of knowledge, allowing some assessment as to whether asymptomatic transmission might be considered beneficial in that it induces immunity with a low cost in disease burden, thus enhancing herd immunity, or detrimental in that it fuels untracked transmission and facilitates the evolution of vaccine escape variants and carries the risk of long COVID. What has been less clear and currently remains unresolved is the nature of the immune determinants that dictate why, after a similar viral inoculum, some individuals will develop no detectable symptoms, others will develop mild symptoms and yet others will develop severe or fatal symptoms. The first point we discuss is the role of immune recognition of the virus during asymptomatic infection - it is certainly clear that innate and adaptive immune activation are triggered during even the mildest infection. We then discuss current insights into innate and adaptive immunity in asymptomatic infection, an area which is very much a work in progress, yet with massive ramifications. If, on the other hand, it is an invisible precursor to long-term disease, it should be a cause of great concern. If there is no health cost to asymptomatic infection, there is no need to fear it or count it, and it could indeed serve it as a natural top-up to SARS-CoV-2 immunity. More data are urgently needed, but whether or not asymptomatic infection poses a risk similar to that posed by symptomatic infection with regard to long-term complications is clearly a decisive question. We then discuss the preliminary evidence that asymptomatic infection is similar to mild or severe COVID-19 in its ability to trigger long-term, persistent symptoms termed ‘long COVID’. We start by considering the now well-established data showing that asymptomatic presentation is relatively common and is a major route of transmission - a key point in the past year’s steep learning curve in attempts to explain the rapid spread of the virus, which necessitated a complex reappraisal of pre-emptive mitigation strategies. For this Progress article, we aim to build a picture of the emergent field of the immunology of asymptomatic infection. As with so many other aspects of medical research in the time of COVID-19, the pandemic has fast-tracked us into deploying our skillsets to address completely new questions. Our natural territory is understanding the mechanism underlying severe infection and protection against it. Although studies such as this established the likelihood of asymptomatic transmission, a mass screening study from Luxembourg at the end of 2020 formally demonstrated that asymptomatic carriers infect a similar number of people to symptomatic individuals 8.Īsymptomatic infection is a tricky and uncharted territory for infectious disease immunologists and clinicians. Asymptomatic COVID-19 case-finding depends on regular community screening by PCR-based approaches and/or serology, either in a cohort study setting 6, 7 or to trace potential transmission after possible exposure, as in the care home example. Asymptomatic transmission was thus described as the “Achilles’ heel” of SARS-CoV-2 infection control strategies 1. An account of a COVID-19 outbreak in a US care home in April 2020 described how one positive case led to 63% of residents becoming infected, although half of these had asymptomatic infections that would not have been identified except by regular PCR testing 5. In retrospect, it became apparent that a significant proportion of infections with MERS-CoV are asymptomatic 4, but this virus is significantly less infectious than SARS-CoV-2. Thus, surveillance and case-finding would require far greater resources and vigilance than previously thought for example, temperature monitoring is not sufficient to detect all individuals infected with SARS-CoV-2. Early in the COVID-19 pandemic it became clear that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) would pose greater challenges to infection control than infection with SARS-CoV in 2002–2003 or Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012, as SARS-CoV-2 is spread readily between people, even by those who are presymptomatic or asymptomatic 1, 2, 3.
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