Feline morbillivirus (FmoPV) is an emerging virus in cats, which is associated
with tubulointerstitial nephritis. To study the in vitro host range of
FmoPV, we inoculated FmoPV strain SS1 to 32 cell lines originated from 13 species and
cultured for 2 weeks, followed by RNA extraction and reverse-transcription-polymerase
chain reaction for FmoPV detection. As a result, only cell lines derived from cats and
African green monkeys were susceptible to FmoPV. FmoPV infects diverse feline cell lines:
epithelial, fibroblastic, lymphoid and glial cells. These results indicate that the
receptor (s) for FmoPV are ubiquitously expressed in cats. No infectivity of FmoPV was
observed in human cell lines, which suggests least threatening of cross-species
transmission of FmoPV from cats to humans.
Feline morbillivirus (FmoPV) is an emerging virus that was recently discovered
in domestic cats with chronic nephritis. Despite the potential role of FmoPV in chronic
nephritis, little is known about its biological characteristics. In this study, we
established a quantitative assay of FmoPV by using an indirect immunofluorescence
technique. Viral titers of FmoPV were determined in one week. Treatment with
polybrene® or trypsin which was previously used in virus isolation did not
augment the virus titers. FmoPV was notably stable at 4°C, retaining high titers for at
least 12 days. Heat-treatment at 60°C and 70°C effectively inactivated FmoPV in 10 and 2
min, respectively. The biological characteristics of FmoPV reported here will be
beneficial for establishing an efficient virus isolation method and will provide important
information to take a measure to reduce the risk of FmoPV infection.
Sequences homologous to human herpesvirus 6 (HHV-6) are integrated within the nuclear genome of about 1% of humans, but it is not clear how this came about. It is also uncertain whether integrated HHV-6 can reactivate into an infectious virus. HHV-6 integrates into telomeres, and this has recently been associated with polymorphisms affecting MOV10L1. MOV10L1 is located on the subtelomere of chromosome 22q (chr22q) and is required to make PIWI-interacting RNAs (piRNAs). As piRNAs block germline integration of transposons, piRNA-mediated repression of HHV-6 integration has been proposed to explain this association. In vitro, recombination of the HHV-6 genome along its terminal direct repeats (DRs) leads to excision from the telomere and viral reactivation, but the expected "solo-DR scar" has not been described in vivo. Here we screened for integrated HHV-6 in 7,485 Japanese subjects using whole-genome sequencing (WGS). Integrated HHV-6 was associated with polymorphisms on chr22q. However, in contrast to prior work, we find that the reported MOV10L1 polymorphism is physically linked to an ancient endogenous HHV-6A variant integrated into the telomere of chr22q in East Asians. Unexpectedly, an HHV-6B variant has also endogenized in chr22q; two endogenous HHV-6 variants at this locus thus account for 72% of all integrated HHV-6 in Japan. We also report human genomes carrying only one
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