Genome Sequence of a Human Tumorigenic Poxvirus: Prediction of Specific Host Response-Evasion Genes

Abstract

Molluscum contagiosum virus (MCV) commonly causes asymptomatic cutaneous neoplasms in children and sexually active adults as well as persistent opportunistic acquired immunodeficiency syndrome (AIDS)-associated disease. Sequencing the 190-kilobase pair genome of MCV has now revealed that the virus potentially encodes 163 proteins, of which 103 have homologs in the smallpox virus. MCV lacks counterparts to 83 genes of the smallpox virus, including those important in suppression of host responses to infection, nucleotide biosynthesis, and cell proliferation. MCV possesses 59 genes that are predicted to encode previously uncharacterized proteins, including major histocompatibility complex class I, chemokine, and glutathione peroxidase homologs, which suggests that there are MCV-specific strategies for coexistence with the human host.

The genome of pseudocowpoxvirus: comparison of a reindeer isolate and a reference strain

“…G+C genome profiles of PCPV strains F00.120R and VR634, ORFV strain NZ2, BPSV strain AR02 and Molluscum contagiosum virus (MOCV) (GenBank accession no. U60315) (Senkevich et al, 1996). Each trace represents the percentage of G+C content of the viral genomes.…”

Evolution of HIV-1-related conjunctival molluscum contagiosum under HAART: report of a bilaterally manifesting case and literature review

“…In contrast to other poxviruses, MC invokes but a poor cellmediated immune response [52], an observation that has been corroborated at the molecular level. Senkevich et al [52] demonstrated that of the 163 potential proteins encoded by the MC genome, 103 have homologues in the variola (smallpox) virus; however, MC lacks almost all of the variola virus genes that are responsible for host-virus interaction.…”

“…MC infections received little attention until the advent of the AIDS epidemic, when extensive and recalcitrant MC lesions emerged as an important cause of disfigurement and morbidity [9,31,33,51]. MC most closely resembles variolae vaccinus, sharing its characteristic ability to replicate entirely within the cytoplasm [36], and the feature of the restricted host range, with man being the only natural host that can support virus replication [36,52]. Ocular manifestations of MC cover a broad spectrum.…”

Tumorigenic poxviruses: growth factors in a viral context?

“…MGF could not replace SFGF, indicating that the latter possesses specific biological activities that are necessary for the complete phenotypic expression of SFV. However, viral growth factors cannot explain all the morphological aberrations observed with tumorigenic poxviruses because: (i) when SFGF is not expressed by SFV, some cellular morphological modifications are still present; (ii) two strains of SFV (Kasza and Boerlage), although possessing identical growth factors, have different clinical outcomes in the European rabbit; and (iii), more importantly, no growth factor homologue was found in MCV or YMTV (Senkevich et al, 1996(Senkevich et al, , 1997Brunetti et al, 2003). For these viruses, it is possible that there are mechanisms in which ErbB receptors or homologues are activated.…”

“…Indeed, it was proposed that EGF homologues are responsible for poxvirus tumorigenesis (Marechal & Piolot, 1999), despite the fact that neither vaccinia virus nor MV is tumorigenic. Moreover, no such homologue has been found in YMTV or MCV (Senkevich et al, 1996;Brunetti et al, 2003).…”