There’s recently been a drastic rise in coronavirus infections among young adults in the US. People in their 20s, 30s, and 40s represent roughly half of cases in coronavirus hot spots like Arizona and Texas, while people ages 18 to 34 represent more than a third of cases in Florida and California.
While SARS-CoV-2 is known to cause substantial pulmonary disease, including pneumonia and acute respiratory distress syndrome (ARDS), clinicians have observed many extrapulmonary manifestations of COVID-19. Our clinical experience and the emerging literature suggest that the hematologic, cardiovascular, renal, gastrointestinal and hepatobiliary, endocrinologic, neurologic, ophthalmologic, and dermatologic systems can all be affected (Supplementary Table)2,3,4,5,6. This pathology may reflect either extrapulmonary dissemination and replication of SARS-CoV-2, as has been observed for other zoonotic coronaviruses7, or widespread immunopathological sequelae of the disease.
There is an urgent need for vaccines to the 2019 coronavirus (COVID19; SARS-CoV-2). Vaccine development may not be straightforward, due to antibody-dependent enhancement (ADE). Antibodies against viral surface proteins can, in some cases, increase infection severity by ADE. This phenomenon occurs in SARS-CoV-1, MERS, HIV, Zika, and dengue virus infection and vaccination. Lack of high-affinity anti-SARS-CoV-2 IgG in children may explain the decreased severity of infection in these groups. Here, we discuss the evidence for ADE in the context of SARS-CoV-2 infection and how to address this potential translational barrier to vaccine development, convalescent plasma, and targeted monoclonal antibody therapies.