Identification and characterization of a type III Trichomonas vaginalis virus in the protozoan pathogen Trichomonas vaginalis

Abstract

A type III Trichomonas vaginalis virus, which may be involved in transcriptional regulation of the major surface protein gene P270 of the protozoan pathogen Trichomonas vaginalis, was purified and characterized in the present study. The complete 4844-base-pair complementary DNA sequence of the viral genome reveals overlapping cap and pol genes with a putative ribosomal frame-shifting signal within the overlap region. The type III virus is related more closely to the type II virus than to the type I virus in the sequence of its ribosomal frameshift signal and in its capsid protein. Phylogenetic analysis revealed that these viruses could be grouped in the same clade as a genus distantly related to other genera in the family Totiviridae. Virus-induced P270 gene expression was only evident in Trichomonas vaginalis cells infected with either a type II or type III virus, but not with a type I virus. These findings suggest that transcription of the P270 gene is likely regulated by viral factors common to type II and type III viruses and thus provides important information for future investigation of virus-host interactions.

Clinical Isolates of Trichomonas vaginalis Concurrently Infected by Strains of Up to Four Trichomonasvirus Species (Family Totiviridae)

“…These T. vaginalis viruses (TVVs) form isometric viral particles (4-6, 15, 41-43) that contain a nonsegmented, 4,500-to 5,000-bp dsRNA genome encoding a viral capsid protein (CP) and a viral RNA-depen-dent RNA polymerase (RdRp) in 2 overlapping open reading frames (ORFs) (5,6,41). The CP ORF is expressed as an independent protein, whereas the RdRp ORF is expressed only as part of a CP/RdRp fusion protein following either a Ϫ1 or a ϩ1 ribosomal frameshifting mechanism before termination of the CP ORF (5,6,26,41). This fusion protein is also incorporated into viral particles at low levels (5,26) and permits these particles to mediate viral RNA synthesis, both transcription and replication (24).…”

“…Transmission of TVV instead occurs upon cell division and possibly also during mating (27). Despite their nonlytic life style, infection by certain TVVs has been shown to alter the surface expression of a highly immunogenic T. vaginalis protein, P270 (6,23,45), as well as the expression profiles of cysteine proteinases that are known virulence factors (32). Thus, infection of T. vaginalis by TVVs could very conceivably modulate the pathogenicity of T. vaginalis infections of the human genital mucosa.…”

“…To date, the near-complete cDNA sequences of only 5 TVV strains (5,6,25,40,41), plus the protein-encoding portions of a sixth strain (51), have been reported to GenBank. Based on these sequences, phylogenetic comparisons have contributed to the recent creation of a new genus in the family Totiviridae, designated Trichomonasvirus, to accommodate these viruses (20).…”

“…Based on these sequences, phylogenetic comparisons have contributed to the recent creation of a new genus in the family Totiviridae, designated Trichomonasvirus, to accommodate these viruses (20). Accompanying the creation of this new genus has been the formal recognition of 3 distinct trichomonasvirus species, designated Trichomonas vaginalis virus 1, Trichomonas vaginalis virus 2, and Trichomonas vaginalis virus 3 (5,6,20,41). Only single strains of the second and third species have been reported to date (5,6).…”

The cell survival pathways of the primordial RNA-DNA complex remain conserved in the extant genomes and may function as proto-oncogenes

“…The heavily duplicated trichomonas genome accepts and rejects horizontally transferred genes of prokaryotic derivation [40], carries dsRNA and totiviridae genomes [41][42][43], harbors inserted retrotransposons (Tc1/ mariner, Kolobok) [44,45], and practices morphological transformation of a fl agellate entity into an amoeboid parasite [46,47].…”