<P> The term viral tropism refers to which cell types EBV infects . EBV can infect different cell types, including B cells and epithelial cells . </P> <P> The viral three - part glycoprotein complexes of gHgL gp42 mediate B cell membrane fusion; although the two - part complexes of gHgL mediate epithelial cell membrane fusion . EBV that are made in the B cells have low numbers of gHgLgp42 complexes, because these three - part complexes interact with Human - leukocyte - antigen class II molecules present in B cells in the endoplasmic reticulum and are degraded . In contrast, EBV from epithelial cells are rich in the three - part complexes because these cells do not normally contain HLA class II molecules . As a consequence, EBV made from B cells are more infectious to epithelial cells, and EBV made from epithelial cells are more infectious to B cells . Viruses lacking the gp42 portion are able to bind to human B cells but unable to infect . </P> <P> EBV can infect both B cells and epithelial cells . The mechanisms for entering these two cells are different . </P> <P> To enter B cells, viral glycoprotein gp350 binds to cellular receptor CD21 (also known as CR2). Then, viral glycoprotein gp42 interacts with cellular MHC class II molecules . This triggers fusion of the viral envelope with the cell membrane, allowing EBV to enter the B cell . Human CD35, also known as complement receptor 1 (CR1), is an additional attachment factor for gp350 / 220, and can provide a route for entry of EBV into CD21 - negative cells, including immature B - cells . EBV infection downregulates expression of CD35 . </P>

Where does human herpesvirus 4 (ebv) become latent