Severe atypical hand-foot-and-mouth disease in adults due to coxsackievirus A6: Clinical presentation and phylogenesis of CV-A6 strains.

BACKGROUND: Typically, hand-foot-and-mouth disease (HFMD) is a mild childhood illness associated with coxsackievirus (CV)-A16, CV-A6, enterovirus (EV)-A71. OBJECTIVES: To identify the viral agents associated with severe cases of atypical HFMD in Italy. STUDY DESIGN: Epidemiologically unrelated cases of severe atypical HFMD admitted to the Emergency Room (ER) of IRCCS San Martino IST (Genoa, Italy) in 2014-2016 were investigated. Serologic screening for viral positivity was performed against exanthem-inducing agents. Ten cases with serology indicative of recent EV infection were selected. Molecular assays were used to detect viral genomes in blood [EVs, Parvovirus B19 (PVB19), herpesviruses (CMV; EBV, HHV-6, -7, -8)]. RESULTS: CV-A6 was detected in 10 cases of severe atypical HFMD. Two cases were also infected with PVB19. Herpesviruses were not detected. Phylogenetic analysis mapped the CV-A6 strains into a single cluster related to two recent isolates from a German and an Asian child. Fever, systemic symptoms, severe vasculitis-like rash, and enanthem were predominant at presentation. Spontaneous recovery occurred in 1-3 weeks. CONCLUSIONS: CV-A6 is emerging as a frequent cause of severe atypical HFMD in Italian adults. This viral agent is disseminating worldwide. Dermatologists must identify the manifold alterations caused by EVs and understand the diagnostic power of current virology methods.

[An oligonucleotide microarray for detection and discrimination of orthopoxviruses based on oligonucleotide sequences of two viral genes].

An oligonucleotide microarray for detection and identification of orthopoxviruses was developed. Genus specific and orthopoxvirus species-specific regions of the genes encoding chemokine binding and alpha/beta-interferon binding proteins were used as a target. The developed microarray allows the variola, monkeypox, cowpox, vaccinia, camel-pox and ectromelia (mousepox) viruses to be distinguished with a high degree of reliability.

Cloning of E6 and E7 genes of human papilloma virus type 18 and transformation potential of E7 gene and its mutants.

E6 and E7 genes of human papilloma virus type 18 have been subcloned from plasmid pC7, carrying an insert of DNA from squamous cell carcinoma of cervix. Both genes in comparison to prototype variant contain one mutation that changes asparagine to leucine. In the case of E6 gene this mutation is mapped in codon 129, in the case of E7 the same change AAC to AAA mapped in codon 92. In addition both genes contain few point mutations that do not change the aminoacid sequences of the protein. Two mutants of E7 gene have been constructed by site directed mutagenesis based on PCR technology-one in codon 10 (change Asp to Asn) and one in codon 24 (change Asp to Gly). The first type of mutation did not influence the transformation potential of the E7 gene in comparison to the parental one with mutation in codon 92. The mutation in codon 24 (region responsible for the interaction with Rb protein) eliminate the transformation potential of the gene. The cells transformed with E7 mutants in codons 10 and 92 were tumorigenic for syngenic rats.