All these issues may have potentially biased our results in 2 selleck chemical Belinostat opposite directions. On one hand we might have overestimated the number of cases, as one or more of suspect cases might actually be prevalent cases who lost anti-HBcAg/anti-HBsAg through severe immunosuppression (false negative) and eventually tested positive after immune reconstitution (potential misclassification). On the other end, we might have underestimated the actual number of cases, in fact, additional case(s) belonging to the reported cluster or even whole additional cluster(s) might have passed thorough unrecognized because of the large number of patients with no information about HBV status (potential misclassification). The results of the inferential study (case-control) might be biased because we included only patients for whom we could define the pre-admission HBV sero-status (potential selection bias).
However this is quite unlikely as there is no reason for a systematic difference between exposure to risk factors and availability of pre-admission HBV sero-status. Given the small number of cases (low inferential power) we could not carry out a multivariate analysis and define other potential risk factor associated with the transmission. Despite the above limitations this study provided, for the first time, molecular evidence to relate the use of one multi-patient lancing device to one HBV infection cluster. This evidence strongly supports the need to remove all shared pricking devices from HCS in order to avoid the occurrence of similar events. Footnotes Competing Interests: The authors have declared that no competing interests exist.
Funding: This study was funded by grants from the Italian Ministry of Health (��Ricerca Corrente IRCCS Lazzaro Spallanzani��) and the Regional Reference Centre for Healthcare-related infections (Centro di Riferimento per le Infezioni associate alle Pratiche Assistenziali della Regione Lazio �C CRIPA-Lazio). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Hepatitis C virus (HCV) is a hepatotropic, positive-strand RNA member of the Flaviviridae family [1]. Approximately 170 million people worldwide are infected with HCV. A notable feature of the virus is its tendency to cause chronic infection. Only a minority of infected patients is able to eradicate the virus, and up to 80% of the patients become chronic carriers.
The molecular mechanisms leading to viral persistency and its ability to evade intracellular host defenses are multi-fold and only partly understood [2]. Currently, there is no effective vaccine against HCV and AV-951 anti-viral therapy has limited efficacy [3]. Similar to other positive-strand RNA viruses, HCV replication involves the formation of a membrane associated replication complex [4].