If dual infections occur with two SARS-CoV-2 viruses, will recombination result in more contagious or deadly variants?

Persistent infection with one SARS-CoV-2 virus in a person with an autoimmune disease receiving extensive immunosuppression, was documented in detail last month by more than 30 authors from Boston. This patient also had “accelerated viral evolution”, with mutations particularly in the spike (S) protein (57%), including the receptor-binding domain.

SARS-CoV-2 variants with multiple mutations in the spike protein and its receptor binding domain have been widely reportedly since last month. These include “B.1.1.7” (first linked with the UK), “B.1.351 (first linked with South Africa) and P.1. (first linked with Brazil). One hypothesis to explain development of such variants is persistent infection in immunocompromised patients, perhaps after receiving convalescent plasma with multiple antibodies to SARS-CoV-2.

In contrast to persistent infections with a single virus, it is not certain that dual infections with genetically-distinct SARS-CoV-2 viruses occur. If dual infections do occur, however, a reasonable hypothesis would be that they are most likely in immunocompromised persons.

If dual infections (overlapping in time) do occur, then would the two viruses be able to recombine and result in a third “offspring” or “progeny” virus that would be more contagious or more deadly, or both?

One of several potential ways to address this question is by focusing on immunocompromised persons while sequencing viruses looking for dual infections. A second focus would be sequencing viruses from persons with unusually rapid clinical progression to severe disease or death.