Persistence of cytomegalovirus in human lymphoblasts and peripheral leukocyte cultures

Abstract

The in vitro susceptibility of human peripheral lymphocytes and lymphoblastoid (F265) cells to infection by human cytomegalovirus was examined. Infection of these cell types with cytomegalovirus resulted in a persistent type of infection rather than the typical growth curve observed with permissive fibroblastic cells. When infection of peripheral lymphocytes was associated with a blastogenic response, the virus persisted for a longer time and at a higher titer than in cells in which a blastogenic response did not occur. Autoradiographic studies and infectious-center assays indicated that only a small number of cells, resembling lymphocytes, were involved in virus persistence. Whether or not the persistence of the virus indicates release of input virus or synthesis of new virus was not determined.

Human cytomegalovirus persists in myeloid progenitors and is passed to the myeloid progeny in a latent form

“…The susceptibility of PBM to HCMV infection has been demonstrated in vitro (Rice et al, 1984;Scott et al, 1989;Rubin, 1990;Söderberg et al, 1993) and in vivo (Danker et al, 1990;Slobedman & Mocarski, 1999). Latently-infected haematopoietic cells may be a source of the HCMV reactivation that occurs in immunodeficient patients (St Jeor & Weisser, 1977;Rice et al, 1984;Drew, 1988;Danker et al, 1990).…”

Sjögren's syndrome: no demonstrable association by serology of secondary Sjögren's syndrome with cytomegalovirus

“…The association with EBV may however, be a con.sequcnce of EBV reactivation subsequent to immune dysregulation, though EBV might play a role in perpetuation of local immune responses in SS (9). CMV has received less attention and yet it infects salivary gland and other tissues (10, II) and stimulates B cell proliferation (12,13), prominent in SS. Studies of CMV in patients with SS have produced equivocal results with, in SS-I, raised IgG and IgM serum antibodies to CMV assayed by an enzyme linked immunosorbent assay (ELISA) (14) and complement fixation assay (15), but no increase in titer of serutn CMV antibodies assayed by radioimmunoassay (RIA) (16) and, in SS-2 normal levels of complement-fixing serum antibodies (15).…”