Summary auto-generated
This study investigated whether oligodendrocytes, brain cells that produce myelin, can be infected with human cytomegalovirus (CMV). The researchers used the HOG cell line, which resembles immature oligodendrocytes, and compared it to U373-MG astrocytoma cells that are known to support full CMV infection. Untreated HOG cells showed incomplete CMV gene expression and no infectious virus production, despite expressing early viral genes in about 40-50% of cells. However, when HOG cells were pretreated with either phorbol 12-myristate 13-acetate (PMA) or dibutyryl cAMP combined with the phosphatase inhibitor IBMX, they became fully permissive to CMV infection, producing infectious viral particles and expressing both early and late viral genes. Only under permissive conditions did CMV-infected HOG cells downregulate HLA class I surface expression, a known immune evasion mechanism. Notably, CMV infection did not upregulate complement regulatory proteins on HOG cells, unlike in other cell types. These findings demonstrate that while immature oligodendrocytes are not fully permissive to CMV, cellular differentiation can enable productive viral infection and replication.
Key findings
- Untreated HOG oligodendroglioma cells support incomplete CMV infection with early gene expression but no infectious virus production
- Chemical differentiation with PMA or dbcAMP/IBMX renders HOG cells fully permissive to CMV, enabling late gene expression and infectious virus production at 10^3-10^4 p.f.u.
- CMV-induced HLA class I downregulation occurs only in permissively infected HOG cells, consistent with viral immune evasion mechanisms
- Unlike in astrocytes, CMV infection does not upregulate complement regulatory proteins CD55 and CD46 on oligodendrocytes, suggesting cell-type-specific viral responses
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Abstract
The well-characterized human oligodendroglioma (HOG) cell line, cells of which resemble immature oligodendrocytes, was used to investigate the level of permissiveness to human cytomegalovirus (CMV) infection. Expression of CMV genes was incomplete following exposure of HOG cells to CMV, in contrast with results observed with the astroglioma cell line U373-MG (used as a positive control). However, treatment with phorbol 12-myristate 13-acetate (PMA) or with dibutryl cAMP (dbcAMP) plus the phosphatase inhibitor 1-isobutyl-3,3-methyl xanthine (IBMX) rendered the HOG cells fully permissive to CMV; down-regulation of HLA class I and production of virions were only observed under these conditions. In contrast to the findings seen with the HOG cell line, treatment of U373-MG cells with dbcAMP/IBMX or PMA did not interfere with CMV-induced down-regulation of HLA class I. However, these chemical stimulators reduced virus production in U373-MG cells by 30 and 70%, respectively.