Human Respiratory Syncytial Virus Infection in a Human T Cell Line is Hampered at Multiple Steps

Human Respiratory Syncytial Virus (HRSV) is a leading cause of acute respiratory infections in humans, more so in infants, the elderly and immunocompromised individuals. HRSV-cell interactions have been studied using epithelial cells. HRSV-cell interaction was studied using lymphoid cells. Although the viral-cell attachment of HRSV to Hep-2 and A3.01 cells is only slightly different, viral genome replication and protein production is greatly reduced in A3.01 cells compared to Hep-2 cells. While there is a clear colocalization between HRSV F protein and Golgi markers in Hep-2 cells, HRSV F protein shows partial colocalization with Golgi markers in A3.01 cells. Although HRSV proteins were readily detected in intracellular compartments of A3.01 cells, very little accumulation of HRSV products was seen at the plasma membrane, which resulted in a lower filament production in these cells. This study suggests that viral replication in A3.01 cells is altered at several stages, including virus-cell fusion, formation of defective inclusion bodies, impaired viral protein production and lack of effective trafficking of viral proteins to virus assembly sites.
(MRM)