Host and Viral Factors in Respiratory Syncytial Virus Infection

Abstract

Respiratory syncytial virus (RSV) is a major worldwide pathogen for which there is still no effective vaccine or antiviral treatment available, and immunoprophylaxis with RSV-specific antibodies (e.g., palivizumab) is used in limited clinical settings. In this review, we discuss virus-host interactions relevant to RSV pathobiology and how advances in cell and systems biology have accelerated knowledge in this area. We also highlight recent advances in understanding the relationship between RSV bronchiolitis and sequelae of recurrent wheezing and asthma, new findings into an intriguing interaction between RSV and air pollution, and exciting developments toward the goal of realizing a safe and effective RSV vaccine.

Revised recommendations concerning palivizumab prophylaxis for respiratory syncytial virus (RSV)

“…At this point, the viral progeny may start to be released from the cell and continue for approximately 48 hours, or until the cell has been completely destroyed. This latter phase might be preceded by the development of cell syncytia (major cytopathogenic effect of the virus) [ 2 , 3 ].…”

Antiviral Activity of Probenecid and Oseltamivir on Influenza Virus Replication

“…Given the pan-antiviral effects of probenecid, this mechanism of action was addressed because it likely involved a host cell pathway used by more than one virus for replication. Several host factors have been associated with RSV replication, including importin-1, Crm1, cofilin, caveolin, ZNF502, and the serine/threonine protein kinase CK2 [13][14][15][16][17]. In addition, c-Jun N-terminal kinase (JNK) activity is known to be required for RSV replication [18].…”

Dynamics and Heterogeneity of mRNA Translation and RNA Virus Infections

“…Defining the factors required for attachment has been complicated by the discrepancy between in vitro and in vivo studies. RSV readily infects cultured cells, whereas infection in the respiratory tract is mostly limited to ciliated epithelial cells (Mastrangelo and Hegele, 2013). Heparan sulfate is a possible explanation for this difference; it is absent on airway epithelial cells in vivo, whereas it is present in high levels on the surface of cultured cells, where it binds well with glycoprotein (G).…”