Characteristics of inactivated hepatitis A vaccine prepared from virus propagated in heteroploid continuous monkey cell line

Kusov, Yu. Yu.; Kazachkov, Yu.A.; Elbert, L. B.; Krutyanskaya, G.L.; Poleschuk, Valentina F.; Sobol, A.V.; Titova, I P; Lisitsyna, E. A.; Drozdov, S. G.; Balayan, M. S.

doi:10.1016/0264-410x(90)90272-n

Cited by 6 publications

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“…In immune-compromised or chronically infected patients, fulminant hepatic failure is often associated with a high mortality rate (15,52). Albeit vaccines against hepatitis A virus can prevent the disease (3,14,31), they are futile for fulminant hepatitis. Therefore, therapeutic intervention strategies to prevent progression to a life-threatening liver disease are still in need.…”

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Silencing of Hepatitis A Virus Infection by Small Interfering RNAs

Kusov

Palmenberg

Sgro

et al. 2006

J Virol

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Infection by hepatitis A virus (HAV) can cause acute hepatitis and, rarely, fulminant liver failure, in particular in patients chronically infected with hepatitis C virus. Based on our previous observation that small interfering RNAs (siRNAs) can silence translation and replication of the firefly luciferase-encoding HAV replicon, we now exploited this technology to demonstrate the effect of siRNAs on viral infection in Huh-7 cells. Freshly and persistently infected cells were transfected with siRNAs targeting various sites in the HAV nonstructural genes. Compared to a single application, consecutive siRNA transfections targeting multiple sequences in the viral genome resulted in a more efficient and sustained silencing effect than a single transfection. In most instances, multiple applications of a single siRNA led to the emergence of viral escape mutants with mutated target sites that rendered these genomes resistant to RNA interference (RNAi). Efficient and sustained suppression of the viral infectivity was achieved after consecutive applications of an siRNA targeting a computer-predicted hairpin structure. This siRNA holds promise as a therapeutic tool for severe courses of HAV infection. In addition, the results provide new insight into the structural bases for sequencespecific RNAi.Hepatitis A virus (HAV) has a single-stranded RNA genome of 7.5 kb with positive polarity. As a member of the picornavirus family, it is unique in its biological properties, in particular, in its highly protracted replicative cycle in cell cultures and inability to shut off the host cell metabolism. HAV causes a self-limiting infection of the liver with usually mild or no symptoms in young patients, whereas adult patients might suffer from severe symptoms. In immune-compromised or chronically infected patients, fulminant hepatic failure is often associated with a high mortality rate (15, 52). Albeit vaccines against hepatitis A virus can prevent the disease (3, 14, 31), they are futile for fulminant hepatitis. Therefore, therapeutic intervention strategies to prevent progression to a life-threatening liver disease are still in need. Given that the rapid degradation of the HAV genome can ameliorate viral infection and thus prevent fulminant failure, RNA interference (RNAi) based on sequence-specific genome degradation may present a novel and specific therapeutic approach in preventing severe disease progression.Initially demonstrated in Caenorabditis elegans and Drosophila melanogaster, RNAi is now recognized as a valuable tool to silence viral infections (reviewed in references 22, 48, and 50). Among the numerous viruses that have been successfully silenced by RNAi, there are five representatives of the picornavirus family: poliovirus (19,20), human rhinovirus (45), enterovirus 71 (37), foot-and-mouth disease virus (7, 9, 36), and coxsackievirus B3 (1, 40). Recently, we have shown that genome replication of an HAV replicon can be efficiently inhibited by small interfering RNAs (siRNAs) targeting either coding or noncoding regions...

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confidence: 99%

Silencing of Hepatitis A Virus Infection by Small Interfering RNAs

Kusov

Palmenberg

Sgro

et al. 2006

J Virol

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“…Μέχρι σήμερα βρίσκονται στο στάδιο της προκαταρκτικής έρευνας ακόμα δύο τουλάχιστον εμβόλια από αδρανοποιημένο ιό (242,243).…”

Section: β-εμβολια απο ααρ ακοπο Iημειγο 10unclassified

Ανοσογονικοτητα Και Ασφαλεια Εμβολιου Απο Αδρανοποιημενο Ιο Ηπατιτιδας Α

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V oenymrns Τμημοτοε ΝοσηΛευτ ι y-fis Γ.ΠΑΠΑΕΥΑΓΤΕΛΟΥ Hoen/nxfis ΤμιΊμοτοβ ΝοσηΛευτ ι y f,s Λ» ΣΠΑΡΟΙ ΗαβηγητηΒ Τμήμοτοε ΝοσηΛευτ ι y ns ΕΞΕΤΑΣΤΙΚΗ ΕΠΙΤΡΟΠΗ Γ. Ι : ΑΡΒΟΥΝΤΖΗΣ Η.ο on ynrns ΤμΛμυΤοκ ΝοσηΛευτ ι κ ns Γ.ΠΑΠΑΕΥΑΓΓΕΛΟΥ Koenyncns Τμημαχο<3 Νασηλευτ ι * ΙΊΒ Α.ΣΠΑΡΟΣ h υ•ε)Γιγητη5 Τμήματος ΝοσηΛευτι Ηns Λ.ΑΝΘΟΠΟΥΛϋΣ Ανοπλ.Γοβηγητη^ Τμηματοε ΝοσηΛευτι κ Ι,. ΜΑΝΤΑΣ Επ ι y . ΚαβηγηττΊε Τμημοτοε ΝοσηΛευτ ι y fi ΒΙΟΓΡΑΦΙΚΟ ΣΗΜΕΙΩΜΑ Γεννήθηκα στην Πάτρα το 1961. Τέλειωσα το Λύκειο στην Αθήνα το 1979. Τον Οκτώβριο του 1979 πέτυχα στις εισαγωγικές εξετάσεις του Ιατρικού τμήματος της Στρατιωτικής Σχολής Αξιωματικών Σωμάτων στην Θεσσαλονίκη. Αποφοίτησα από την Ιατρική Σχολή του Αριστοτελείου Πανεπιστημίου Θεσσαλονίκης τον Ιούλιο του 1985. Υπηρέτησα σαν εσωτερικός βοηθός στο Ναυτικό Νοσοκομείο Αθηνών ano τον Οκτώβριο του 1985 έως τον Δεκέμβριο του 1986. Παράλληλα φοίτησα στο σχολείο Υπερβαρικής Ιατρικής του Ν. If. Α. Στη συνέχεια από τον Ιανουάριο του 1987 έως τον Ιούνιο του 1988 υπηρέτησα σαν ιατρός σε πλοίο του Πολεμικού Ναυτικού. Τον Ιούνιο του 1988 άρχισα την ειδίκευση μου στην Μικροβιολογία.

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