D. O'Hara et al., Avian reovirus major mu-class outer capsid protein influences efficiency of productive macrophage infection in a virus strain-specific manner, J VIROLOGY, 75(11), 2001, pp. 5027-5035
We determined that the highly pathogenic avian reovirus strain 176 (ARV-176
) possesses an enhanced ability to establish productive infections in HD-11
avian macrophages compared to avian fibroblasts, Conversely, the weakly pa
thogenic strain ARV-138 shows no such macrophagotropic tendency. The macrop
hage infection capability of the two viruses did not reflect differences in
the ability to either induce or inhibit nitric oxide production. Moderate
increases in the ARV-138 multiplicity of infection resulted in a concomitan
t increase in macrophage infection, and under such conditions the kinetics
and extent of the ARV-138 replication cycle were equivalent to those of the
highly infectious ARV-176 strain. These results indicated that both viruse
s are apparently equally capable of replicating in an infected macrophage,
but they differ in the ability to establish productive infections in these
cells. Using a genetic reassortant approach, we determined that the macroph
agotropic property of ARV-176 reflects a post-receptor-binding step in the
virus replication cycle and that the ARV-176 M2 genome segment is required
for efficient infection of HD-11 cells, The M2 genome segment encodes the m
ajor mu -class outer capsid protein (muB) of the virus, which is involved i
n virus entry and transcriptase activation, suggesting that a host-specific
influence on ARV entry and/or uncoating may affect the likelihood of the v
irus establishing a productive infection in a macrophage cell.