Abstract
Feline morbillivirus (FeMV) was identified for the first time in stray cats in 2012 in Hong Kong and, since its discovery, it was reported in domestic cats worldwide. Although a potential association between FeMV infection and tubulointerstitial nephritis (TIN) has been suggested, this has not been proven, and the subject remains controversial. TIN is the most frequent histopathological finding in the context of feline chronic kidney disease (CKD), which is one of the major clinical pathologies in feline medicine. FeMV research has mainly focused on defining the epidemiology, the role of FeMV in the development of CKD, and its in vitro tropism, but the pathogenicity of FeMV is still not clear, partly due to its distinctive biological characteristics, as well as to a lack of a cell culture system for its rapid isolation. In this review, we summarize the current knowledge of FeMV infection, including genetic diversity of FeMV strains, epidemiology, pathogenicity, and clinicopathological findings observed in naturally infected cats.
Highlights
Paramyxoviruses constitute a large group of viruses that are responsible for important diseases in humans and animals [1]
The first case–control study [6] has proposed an association of feline morbillivirus (FeMV) infection with chronic tubulointerstitial nephritis (TIN), the most frequent histopathological finding in feline chronic kidney disease (CKD) [7]
A case–control study proposed a link between FeMV infection and TIN [6], and several studies have been performed to ascertain the association between FeMV infection and feline CKD, leading to controversial conclusions [15,26,29]
Summary
Paramyxoviruses constitute a large group of viruses that are responsible for important diseases in humans and animals [1]. As for other paramyxoviruses, the genome of FeMV conforms to the “rule of six”, since each nucleocapsid protein (N) monomer encapsidates six nucleotides of RNA [30]. The six encoded structural proteins include a matrix protein (M), two RNA-polymerase-associated proteins (the phosphoprotein P and the large protein L), a nucleocapsid protein (N) and two glycoproteins (the hemagglutinin H and the fusion protein F) [33]. The genome is encapsidated in the nucleocapsid, which includes proteins N, P, and L The latter proteins along with the viral RNA form a ribonucleoprotein complex that is responsible for the transcription and the replication steps [34]. These viruses are enveloped by a host plasma membrane-derived lipid bilayer acquired during the budding process. The H glycoprotein is a major determinant for virus–host interactions, being responsible for the virus attachment to the host cellular receptors, triggering the activation of glycoprotein F and fusion peptide exposure
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