Reassortment

Reassortment occurs in viruses with segmented genomes, most classically influenza A virus, which has 8 distinct RNA segments. When a host cell (often pigs or birds, acting as 'mixing vessels') is simultaneously infected with two different influenza strains (e.g., human and avian strains), the progeny virions can package a mixture of gene segments from both parental viruses. This creates a novel virus with a new combination of surface antigens (hemagglutinin and/or neuraminidase), a phenomenon termed antigenic shift. Because the human population has little to no pre-existing immunity to this new antigenic combination, reassortment is the mechanism responsible for major influenza pandemics, such as the 1918 H1N1, 1957 H2N2, 1968 H3N2, and 2009 H1N1 pandemics. This is distinct from antigenic drift, which involves gradual point mutations in the RNA polymerase (which lacks proofreading ability) leading to minor antigenic changes and is responsible for seasonal influenza epidemics. Clinically, antigenic shift via reassortment is far more dangerous than drift because it can produce a virus against which humans have no immunity, enabling rapid global spread. Key testable points: reassortment requires a segmented genome (influenza, rotavirus, reovirus), requires co-infection of a single cell by two strains, is the mechanism of antigenic shift (not drift), and swine are classic intermediate hosts due to having both avian and human-type sialic acid receptors in their respiratory tract.