Molecular simulations predict that while TMPRSS2 should have far greater capacity to process S2′ as a cleavage substrate, Moraxella serine protease (MSP) may be capable of exothermically complexing with S2′ and MSP may persistently bind the resulting cleaved fragments in a manner that could delay or abrogate subsequent viral infection steps, such as syncytia formation. This evidence concerns the gene TMPRSS2 and viral infectious disease.