Identification of Host Factors Required for Archaeal Rudivirus Entry
Interactions between a viral protein and host cell surface receptor initiate viral infection. However, very few receptors for viruses that target the Bacteria and Archaea are known. Deng et al. (p. 10264–10268) identified two Sulfolobus gene clusters that are required for rudivirus SIRV2 entry into Archaea cells. These data suggest the existence of a receptor system used by rudiviruses to attach and internalize into Archaea.
Eradicating the HIV-1 Cofactor LEDGF/p75 from Human Cells
Human LEDGF/p75 tethers viral integrase in the HIV-1 preintegration complex to the chromosomal target. While this function facilitates integration into actively transcribed genes, the function of LEDGF in lentiviral biology is not completely understood. Fadel et al. (p. 9704–9717) used TAL effector nucleases to delete the PSIP gene encoding LEDGF/p75 or the PSIP exons encoding the integrase-binding domain in human cells, including a CD4+ T cell line. HIV-1 replication was markedly impaired in the knockout cells. These data define the function of cellular LEDGF/p75 in HIV-1 infection and highlight a potential therapeutic target.
mRNA Overload during Herpes Simplex Virus Infection
Viruses flood infected cells with viral mRNAs, which potentially overload the host translational apparatus. The herpes simplex virus host shutoff RNase (vhs) destabilizes host and viral mRNAs. Dauber et al. (p. 9624–9632) demonstrate that vhs stimulates translation of viral late mRNAs by preventing mRNA overload during the late stages of infection. Pre-existing cellular and early viral mRNAs stably sequester one or more limiting translation factors, thereby placing late viral mRNAs at a competitive disadvantage in the absence of vhs. This work illuminates the function of virus-mediated mRNA destabilization in herpesvirus infection.
Contribution of Adenosine to Leukocyte Recruitment in Influenza
Severe influenza virus infection can progress to life-threatening, acute lung injury. However, mechanisms underlying this process are poorly understood. Aeffner et al. (p. 10214–10227) demonstrate that the nucleoside adenosine is released into the lungs following infection with influenza A virus. Adenosine is an important factor in promoting migration of leukocytes into the influenza virus-infected lung. Moreover, blocking the adenosine receptor improves lung function in influenza virus-infected mice. This work suggests that the adenosine signaling pathway is a promising therapeutic target for reducing influenza virus severity.
Resistance of Virus-Specific T Cells to Apoptosis
The number of virus-specific T cells in the spleen and lymph nodes decreases due to apoptosis and dissemination to nonlymphoid sites following an acute immune response. Apoptosis-resistant T cells linger in peripheral tissue, possibly to prevent reinfection with the same pathogen. Kapoor et al. (p. 9490–9503) show that T cells in the periphery but not T cells in the spleen display a molecular signature of apoptosis-resistant cells. Chemokines recruit apoptosis-resistant cells away from lymphoid organs and into peripheral tissue, which contains an environment suitable for cell survival.