A systematic approach to virus–virus interactions

Abstract

A virus-virus interaction is a measurable difference in the course of infection of one virus as a result of a concurrent or prior infection by a different species or strain of virus. Many such interactions have been discovered by chance, yet they have rarely been studied systematically. Increasing evidence suggests that virus-virus interactions are common and may be critical to understanding viral pathogenesis in natural hosts. In this review we propose a system for classifying virus-virus interactions by organizing them into three main categories: (1) direct interactions of viral genes or gene products, (2) indirect interactions that result from alterations in the host environment, and (3) immunological interactions. We have so far identified 15 subtypes of interaction and assigned each to one of these categories. It is anticipated that this framework will provide for a more systematic approach to investigating virus-virus interactions, both at the cellular and organismal levels.

Cytomegalovirus reactivation after autologous stem cell transplantation in myeloma and lymphoma patients: A single-center study

“…HBV positive patients could be considered as patients at risk for CMV reactivation [22,23] . The role of a HBV latent co-infection as independent factor for CMV reactivation observed in our study has a physiopathologic rationale, considering that interactions among some different viruses have been demonstrated to have a role in the pathogenesis of infections, through mechanisms of cross-permissiveness mediated by the immune system [14,[24][25][26] . In fact, the mechanisms of virus-virus interaction is common and crucial to understanding pathogenesis of viral infections; we hypothesized that HBV is capable of favoring a CMV co-infection through direct interaction of viral molecules, but also trough acting on cell-mediate immune system [26] .…”

“…The role of a HBV latent co-infection as independent factor for CMV reactivation observed in our study has a physiopathologic rationale, considering that interactions among some different viruses have been demonstrated to have a role in the pathogenesis of infections, through mechanisms of cross-permissiveness mediated by the immune system [14,[24][25][26] . In fact, the mechanisms of virus-virus interaction is common and crucial to understanding pathogenesis of viral infections; we hypothesized that HBV is capable of favoring a CMV co-infection through direct interaction of viral molecules, but also trough acting on cell-mediate immune system [26] . However, contrasting data are recently obtained in allogeneic hematopoietic stem cell transplantation by Lin and collaborators, that suggest that the underlying HBV infection in donors or recipients before transplant does not increase the risk of CMV infection and endorgan disease [27] .…”

Myxomavirus-Derived Serpin Prolongs Survival and Reduces Inflammation and Hemorrhage in an Unrelated Lethal Mouse Viral Infection

“…Both cascades activate inflammatory cell responses: tPA and uPA, via activation of matrix metalloproteinases and growth factors (14,18,36), and thrombin and fX, via activation of proteaseactivated receptors (PARs) (2,3,7,8), increasing inflammatory cell invasion and activation. ⌴HV68 traffics into the lung by 10 to 12 days after injection, with acute infection of lung and persistent infection in B lymphocytes, epithelial cells, and macrophages (26,27).…”

The susceptibility of primary cultured rhesus macaque kidney epithelial cells to rhesus cytomegalovirus strains

“…The reasons for losing the full-length variant after serial passages in MKE are unclear. However, infection with multiple genetically distinct strains of a virus is common in nature and can lead to positive (complementary) or negative (competitive) within-host virus-virus interactions (DaPalma et al, 2010;Read & Taylor, 2001). Given the low frequency (~6.7 %) of the full-length variant in the original Telo-RF-propagated stock, coupled with propagation of the 180.92 stock in MKE at exceedingly low m.o.i.…”