AI Summary
Viruses have co-evolved with living organisms and adapt to infect specific hosts. They rely on specific cellular factors and can infect different cell types within a species. Researchers often study viruses in simplified model systems. Studying viral replication in new environments can help understand virus adaptation. Viruses that infect animals through the gastrointestinal tract must be well adapted to withstand harsh digestive conditions.
INTRODUCTIONViruses are obligate intracellular parasites that have co-evolved with living organisms for millions of years (1). Consequently, each virus species has adapted to infect and hijack the cellular machinery of its natural hosts, whether they be bacteria, plants, or specific cells within animals. The reliance on specific cellular factors available in distinct hosts has been characterized for some viruses (2–4). For example, the preference of avian compared to human strains of influenza A virus for sialic acids with slightly different molecular structures contributes to the host tropism of these strains (3). Additionally, different cell types within a species can express distinct molecular factors essential for some viruses (5–9). The liver-specific microRNA-122, for instance, is essential for hepatitis C virus replication in the liver (9). Despite the long history of viral adaptation, researchers often study viruses using simplified model systems that lack the complexity and diversity found in natural viral infections (7, 10–12). By characterizing molecular features that govern viral replication in new environments, we can better understand how viruses adapt to new hosts or to distinct niches within a given host. Such knowledge could help appreciate virus progression across and within domains of life and could, for example, help predict virus adaptation to new pressures.Viruses that infect animals through the gastrointestinal tract must be, especially, well adapted to withstand harsh digestive conditions, such as pH changes and proteolytic enzymes (13–15). To achieve successful enteric infection, viruses such as rotavirus, mammalian orthoreovirus, and human astrovirus have evolved hyper-stable capsid structures