N. Gogate et al., MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I EXPRESSION ON NEURONS IN SUBACUTE SCLEROSING PANENCEPHALITIS AND EXPERIMENTAL SUBACUTE MEASLES ENCEPHALITIS, Journal of neuropathology and experimental neurology, 55(4), 1996, pp. 435-443
Lack of major histocompatibility class I antigens on neurons has been
implicated as a possible mechanism for viral persistence in the brain
since these antigens are required for cytotoxic T-lymphocyte recogniti
on of infected cells. In subacute sclerosing panencephalitis (SSPE), m
easles virus (MV) persists in neurons, resulting in a fatal chronic in
fection. MHC class I mRNA expression was examined in formalin-fixed br
ain tissue from 6 SSPE patients by in situ hybridization. In addition
MHC class I protein expression in MV-infected neurons was examined in
experimental Subacute Measles Encephalitis (SME) by double immunohisto
chemistry. MHC class I mRNA expression was found to be upregulated in
SSPE tissues studied, and in 5 out of 6 cases the expression was defin
itively seen on neurons. The percentage of neurons expressing MHC clas
s I mRNA ranged between 20 to 84% in infected areas. There was no corr
elation between the degree of infection and expression of MHC class I
molecules on neurons. Importantly, the number of neurons co-expressing
MHC class I and MV antigens was markedly low, varying between 2 to 8%
. Similar results were obtained in SME where 20 to 30% of the neurons
expressed MHC class I but < 8% co-expressed MHC class I and MV antigen
s. Perivascular infiltrating cells in the infected regions in SME expr
essed IFN gamma immunoreactivity. The results suggest that MV may not
be directly involved in the induction of MHC class I on neurons and th
at cytokines such as IFN gamma may play an important role. Furthermore
, the paucity of neurons co-expressing MHC class I and MV antigens in
SSPE and SME suggests that such cells are either rapidly cleared by cy
totoxic T lymphocytes (CTL), or, alternatively, lack of co-expression
of MHC class I on MV infected neurons favors MV persistence in these c
ells by escaping CTL recognition.