Dicistroviridae is a recently established family of small, non-enveloped viruses, containing a +ssRNA genome, and is classified under the order Picornavirales. This family contains 14 members classified within two genera, Cripavirus (type species Cricket paralysis virus, CrPV), and Aparavirus (type species Acute bee paralysis virus, ACP) [1, 2]. A third genus has been recently proposed, Triatovirus (type species Triatoma virus, TrV) . All dicistroviruses are pathogenic to arthropods, although primarily to insects, representing significant threats to the health of beneficial arthropods such as acute bee paralysis virus, Black queen cell virus, Kashmir bee virus, which infects honeybees [4–6], and Taura syndrome virus, which is pathogenic to shrimps . Two dicistrovirus members infect the model organism Drosophila melanogaster, Drosophila C virus (DCV) and CrPV [8, 9], and eight of them are pathogenic to insect pests, as it is the case with CrPV, which infects field crickets and the Olive Fruit Fly as well . The aforementioned CrPV is quite ubiquitous and replicates in many other insect species spanning five orders . Although dicistroviruses are believed to be arthropod-specific, antibodies against CrPV have been detected in sera from a pig, horse, and cattle . Similarly, high levels of anti-TrV antibodies were detected in chickens used to feed a colony of TrV-infected insects, although the authors of this work concluded that the chickens were apparently refractory to the infection with TrV .
Compared to other families of picornaviruses, little is known about dicistrovirus infection, replication mechanism or gene function. Most information about cellular infection and the replication cycle of dicistroviruses comes from studies on DCV, and by comparison with mammalian picornaviruses . Many members of the Dicistroviridae family are considered novel candidates to be used as biopesticides [1, 13–17].
TrV and Solenopsis invicta virus-1 are the two lone members of the Dicistroviridae family that infect insects of medical importance . In fact, TrV is a natural enemy of Triatoma infestans (Hemiptera: Reduviidae), one of the main vectors of the trypanosomiasis disease called Chagas disease, a severe human illness most prevalent in almost all Latin American countries [18, 19]. To date, TrV is the only entomopathogenic virus found in triatomines . The viral particles are spherical, with a diameter of 30 nm , and consist of a non-enveloped capsid that encloses a 9010 nt long viral genome . The capsid contains four structural proteins VP1 (29.7 kDa), VP2 (28.4 kDa), VP3 (31.8 kDa) and a minor one VP0 (37.3 kDa). In addition to these four structural proteins, this virus has a low molecular weight protein of 5.5 kDa that appears to be detached from the capsid, lying at the particle interior and presumably in contact with the genome [3, 20, 23]. TrV can also infect natural populations of T. sordida and several experimental populations of triatomines as well . Viral replication takes place in the midgut epithelium cells of triatomines, causing many deleterious sublethal effects in T. infestans and T. patagonica colonies, such as reduction of the longevity, increase of the developmental time, a decrease in both fecundity and fertility of eggs, and even a cumulative mortality higher than 97% [16, 25–28].
As pointed out previously, the infectivity of TrV in vertebrates remains unclear. Therefore, in this work we studied the infectivity of TrV in mice (Mus musculus - BALB/c mice). Our results indicate that inoculations of both infective and non-infective TrV particles elicit the same immune response, and that this insect virus is unable to replicate in this animal model. Based on the bicistronic character of dicistrovirus genomes, it was speculated that these pathogens may not infect vertebrates, and this report constitutes important experimental evidence to support that hypothesis.