Abstract
Canine distemper virus (CDV) is a highly contagious pathogen transmissible to a broad range of terrestrial and aquatic carnivores. Despite the availability of attenuated vaccines against CDV, the virus remains responsible for outbreaks of canine distemper (CD) with significant morbidity and mortality in domesticated and wild carnivores worldwide. CDV uses the signaling lymphocytic activation molecule (SLAM, or CD150) and nectin-4 (PVRL4) as entry receptors, well-known tumor-associated markers for several lymphadenomas and adenocarcinomas, which are also responsible for the lysis of tumor cells and apparent tumor regression. Thus, CDV vaccine strains have emerged as a promising platform of oncolytic viruses for use in animal cancer therapy. Recent advances have revealed that use of the CDV reverse genetic system (RGS) has helped increase the understanding of viral pathogenesis and explore the development of recombinant CDV vaccines. In addition, genetic engineering of CDV based on RGS approaches also has the potential of enhancing oncolytic activity and selectively targeting tumors. Here, we reviewed the host tropism and pathogenesis of CDV, and current development of recombinant CDV-based vaccines as well as their use as oncolytic viruses against cancers.
Highlights
Canine distemper virus (CDV) is an enveloped negative-RNA virus, which, along with measles virus (MeV), Rinderpest virus (RPV), peste des petits ruminants virus (PPRV), phocine distemper virus (PDV), Cetacean morbillivirus (CeMV), and recently discovered feline morbillivirus (FeMV), belongs to the Morbilivirus genus within the Paramyxoviridae family [1,2]
CDV is the etiological agent of canine distemper (CD) that has been known since the mid-1700s and might have originated from the infection of dogs by MeV during human epidemics in the New World [3]
Several generated reverse genetic system (RGS) have been reported for the rescue of CDV wild-type strains from marmoset lymphoblastoid cells (B95a) or Vero cells expressing the signaling lymphocytic activation molecule (SLAM) receptor (Vero-SLAM) that allows for propagation of wild-type CDVs and maintenance of their virulence in vivo (Figure 1)
Summary
Canine distemper virus (CDV) is an enveloped negative-RNA virus, which, along with measles virus (MeV), Rinderpest virus (RPV), peste des petits ruminants virus (PPRV), phocine distemper virus (PDV), Cetacean morbillivirus (CeMV), and recently discovered feline morbillivirus (FeMV), belongs to the Morbilivirus genus within the Paramyxoviridae family [1,2]. CDV is the etiological agent of canine distemper (CD) that has been known since the mid-1700s and might have originated from the infection of dogs by MeV during human epidemics in the New World [3] Both viral agents are known to be highly contagious, spread via the respiratory route, and cause a similar pathogenesis characterized by fever, skin rash, and conjunctivitis with profound immune suppression, and elicit lifelong immunity in surviving hosts [4,5,6,7]. Persistent infection by CDV has been shown to exhibit anti-angiogenic properties in a canine histiocytic cell line [16,17,18,19,20] These findings suggest that CDV could be used as an oncolytic virus in oncolytic gene therapy in both humans and animals. The vector use of RNA viruses was experimentally encouraged by the pronounced and unexpected genetic stability of the recombinants, and by the high load of insertable genetic material [21]
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