Persistent viremia by a novel parvovirus in a slow loris (Nycticebus coucang) with diffuse histiocytic sarcoma

Abstract

Cancer is one of the leading health concerns for human and animal health. Since the tumorigenesis process is not completely understood and it is known that some viruses can induce carcinogenesis, it is highly important to identify novel oncoviruses and extensively study underlying oncogenic mechanisms. Here, we investigated a case of diffuse histiocytic sarcoma in a 22 year old slow loris (Nycticebus coucang), using a broad spectrum virus discovery technique. A novel parvovirus was discovered and the phylogenetic analysis performed on its fully sequenced genome demonstrated that it represents the first member of a novel genus. The possible causative correlation between this virus and the malignancy was further investigated and 20 serum and 61 organ samples from 25 animals (N. coucang and N. pygmaeus) were screened for the novel virus but only samples collected from the originally infected animal were positive. The virus was present in all tested organs (intestine, liver, spleen, kidneys, and lungs) and in all banked serum samples collected up to 8 years before death. All attempts to identify a latent viral form (integrated or episomal) were unsuccessful and the increase of variation in the viral sequences during the years was consistent with absence of latency. Since it is well known that parvoviruses are dependent on cell division to successfully replicate, we hypothesized that the virus could have benefitted from the constantly dividing cancer cells and may not have been the cause of the histiocytic sarcoma. It is also possible to conjecture that the virus had a role in delaying the tumor progression and this report might bring new exciting opportunities in recognizing viruses to be used in cancer virotherapy.

Driving forces behind the evolution of the Aleutian mink disease parvovirus in the context of intensive farming

“…Six (15%) of the sites under purifying selection identified in NS1 were located in the helicase domain, five of which (sites 432, 433, 434, 438, and 439) were localized in the ATP-binding loop ( Walker et al. 1982 ) as illustrated in Canuti et al. (2014) .…”

Molecular Characterization and Evolutionary Analyses of Carnivore Protoparvovirus 1 NS1 Gene

“…This region includes the convergent mutation between the CPV and FPLV clades (change Q to E in some FPLV strains) at the positively selected site 545 and the only residue subjected to positive selection pressure within the FPLV strains (site 443). Whereas residue 443 putatively lies in the β3-sheet of the Walker motif B of the helicase domain protein sequence, residues 350 and 544–545 are located between the α5- and α6-helices and just close to the α11-helix of the same domain, respectively, as illustrated in Canuti et al [70] and Niskanen et al [23]. The evidence of the convergent or divergent amino-acid changes between FPLV and CPV could contribute to further elucidate NS1 protein structure by clarifying any potential role of these residues.…”

Association of the Human Bocavirus With Tonsil Squamous Cell Carcinomas

“…The majority of known parvoviruses is dependent on the cell cycle and are capable of replicating, probably exclusively, in actively replicating cells (in S phase). For this reason, they thrive in cancerous cells, often giving the false impression of being oncogenic ( Canuti et al, 2014 ). In addition, there is indeed a well-established relationship between cancer and parvoviruses but this is most likely the result of viral replication reactivation in the replicating cancer calls, causing an increased viral load and therefore a higher prevalence in cancer patients, compared to healthy subjects ( Cotmore et al, 2014 ; Kishore and Kishor, 2014 ; Phan et al, 2016 ; Qiu et al, 2017 ).…”