Small Ruminant Lentiviruses (SRLVs) Break the Species Barrier to Acquire New Host Range

Abstract

Zoonotic events of simian immunodeficiency virus (SIV) from non-human primates to humans have generated the acquired immunodeficiency syndrome (AIDS), one of the most devastating infectious disease of the last century with more than 30 million people dead and about 40.3 million people currently infected worldwide. Human immunodeficiency virus (HIV-1 and HIV-2), the two major viruses that cause AIDS in humans are retroviruses of the lentivirus genus. The genus includes arthritis-encephalitis virus (CAEV) and Maedi-Visna virus (MVV), and a heterogeneous group of viruses known as small ruminant lentiviruses (SRLVs), affecting goat and sheep. Lentivirus genome integrates into the host DNA, causing persistent infection associated with a remarkable diversity during viral replication. Direct evidence of mixed infections with these two closely related SRLVs was found in both sheep and goats. The evidence of a genetic continuum with caprine and ovine field isolates demonstrates the absence of an efficient species barrier preventing cross-species transmission. In dual-infected animals, persistent infections with both CAEV and MVV have been described, and viral chimeras have been detected. This not only complicates animal trade between countries but favors the risk that highly pathogenic variants may emerge as has already been observed in the past in Iceland and, more recently, in outbreaks with virulent strains in Spain. SRLVs affecting wildlife have already been identified, demonstrating the existence of emergent viruses adapted to new hosts. Viruses adapted to wildlife ruminants may acquire novel biopathological properties which may endanger not only the new host species but also domestic ruminants and humans. SRLVs infecting sheep and goats follow a genomic evolution similar to that observed in HIV or in other lentiviruses. Lentivirus genetic diversity and host factors leading to the establishment of naturally occurring virulent versus avirulent infections, in addition to the emergence of new strains, challenge every aspect of SRLV control measures for providing efficient tools to prevent the transmission of diseases between wild ungulates and livestock.

Phylogenetic Analysis of Belgian Small Ruminant Lentiviruses Supports Cross Species Virus Transmission and Identifies New Subtype B5 Strains

“…This excess of uracil can be incorporated into the DNA leading to more mutations in newly produced virions (reviewed in [13]). A third source of genetic evolution in lentiviruses that adds to their adaptability and genetic diversity is the occurrence of recombination between strains [26]. This mechanism allows viruses to combine genetic information which can lead to new emerging strains.…”

“…This indicates that cross species transmission from sheep to goats and vice versa has occurred. Cross species transmission of SRLV strains has been reported before [8,27,28] and such transmission events probably occur via transmission of viral particles via the air when different species are in close contact or via feeding of contaminated milk from sheep to goat or vice versa [8,26,29]. Although animal WV.7.1 came from a farm where both sheep and goats were present, our available information does not allow to deduce whether the cross-species transmission has occurred at this farm, or that this strain entered the farm via the purchase of an animal infected with an A1 strain.…”

Archival search for historical atypical scrapie in sheep reveals evidence for mixed infections

“…It is therefore more likely that natural TSE infections of ruminants involve mixtures of strains, or have a more fluid identity, rather than the single strains normally used in laboratory studies. Combinations of infections have been implicated in the development of novel strains with altered host range in lentivirus infections of ruminants (Minardi da Cruz et al, 2013), and such combinations of strains and types of virus/bacteria/prions, particularly in persistent infections, are more likely to represent the real-life situation in the field and could favour the emergence of more highly virulent disease-causing agents. Whereas viruses can recombine their genetic material to form new strains, the concept of the prion being free from any nucleic acid makes it challenging, but also important, to understand how mixed prion strains interact.…”

How does the humoral response to HIV-2 infection differ from HIV-1 and can this explain the distinct natural history of infection with these two human retroviruses?

“…The lentivirus genome integrates into the host DNA, causing persistent infection which is associated with notable genetic diversity, promoted by high rates of mutation and recombination during viral replication. Lentiviruses infect a limited range of mammalian hosts such as humans (HIV), non-human primates (SIV), felines (FIV), cattle (BIV), goats (caprine arthritis encephalitis virus; CAEV) and sheep (Visna virus) [12,34].…”