Effect of antioxidants on apoptosis induced by influenza virus infection: inhibition of viral gene replication and transcription with pyrrolidine dithiocarbamate

Uchide, Noboru; Ohyama, Kunio; Bessho, Toshio; Yuan, Bo; Yamakawa, Toshio

doi:10.1016/s0166-3542(02)00109-2

Cited by 94 publications

(82 citation statements)

References 32 publications

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“…However, any influences of influenza virus infection on a maternal body and on the pregnancy retaining are still unknown. As we demonstrated that the IV-infection induced apoptotic phenomena were associated with viral macromolecular synthesis in host cells, 8) and that a viral constituent, a hemagglutinin resulted in the induction of apoptosis in fetal cells through an oxidative stress production, 9) we investigated the molecular mechanism of the apoptotic induction in human uterine cell line, HCF, caused by influenza virus type A (IV-A) or type B (IV-B) infection for studying apoptotic effect of the infection in maternal body and some roles of the apoptosis induction in its defense mechanism.…”

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confidence: 77%

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Predominant Contribution of IFN-.BETA. Expression to Apoptosis Induction in Human Uterine Cervical Fibroblast Cells by Influenza-Virus Infection

Ohyama

Sano

Toyoda

2004

Biological & Pharmaceutical Bulletin

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confidence: 77%

“…1) The chorioallantoic fluid contained 8ϫ10 8 plaque-forming units (PFU)/ml of both type of viruses and the hemagglutination titer of both virus solutions using 1% chicken erythrocytes in PBS solution was 1/256.…”

Section: Methodsmentioning

confidence: 99%

Predominant Contribution of IFN-.BETA. Expression to Apoptosis Induction in Human Uterine Cervical Fibroblast Cells by Influenza-Virus Infection

Ohyama

Sano

Toyoda

2004

Biological & Pharmaceutical Bulletin

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“…PDTC was shown to be a potent inhibitor of the multiplication of HRV and poliovirus, both members of the Picornaviridae (11). Furthermore, PDTC turned out to prevent the multiplication of influenza virus, belonging to the Orthomyxoviridae (48). This indicates that the antiviral effect of PDTC is not restricted to one distinct virus family, and thus its mode of action might rely on more general mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Polyprotein Processing and RNA Replication of Human Rhinovirus by Pyrrolidine Dithiocarbamate Involves Metal Ions

Krenn

Holzer

Gaudernak

et al. 2005

J Virol

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Pyrrolidine dithiocarbamate (PDTC) is an antiviral compound that was shown to inhibit the replication of human rhinoviruses (HRVs), poliovirus, and influenza virus. To elucidate the mechanism of PDTC, the effects on the individual steps of the infection cycle of HRV were investigated. PDTC did not interfere with receptor binding or internalization by receptor mediated endocytosis of HRV2 particles into HeLa cells. But we demonstrate that the processing of the viral polyprotein was prevented by PDTC treatment in HeLa cells infected with HRV2. Furthermore, PDTC inhibited the replication of the viral RNA, even when added four hours post infection. As PDTC is described as a metal ion binding agent, we investigated the effect of other metal chelators on the multiplication of HRV2. We show that EDTA, -phenanthroline, and bathocuproine disulfonic acid do not exhibit any antiviral properties. Surprisingly, these substances, coadministered with PDTC, abolished the antiviral effect of PDTC, suggesting that metal ions play a pivotal role in the inhibition of virus multiplication. These results suggest that PDTC inhibits the activity of the viral proteases in a metal ion dependent way.Human rhinoviruses (HRVs) are the most frequent cause of the common cold and are implicated in more than 50% of upper respiratory tract infections (45). Although not life threatening, infection with HRV can prepare the ground for more serious diseases, such as acute exacerbation of asthma (20, 30) or otitis media (5). As there are more than 100 HRV serotypes, vaccine development is unfeasible. Apart from symptomatic medication no causative treatment for HRV infections is currently available. Therefore, analysis of functions of new antiviral substances is of great interest and might also shed light on novel aspects of virus-cell interactions.HRVs belong to the genus Picornaviridae. These viruses have a single-stranded positive-sense RNA genome of approximately 7,400 nucleotides. The viral RNA encodes four capsid proteins (VP1 through VP4) and seven nonstructural proteins that are involved in viral RNA replication and polyprotein processing. The HRV serotypes can be classified into A and B groups based on sequence alignments (36). Alternatively, HRVs are divided into two groups according to their receptor specificity (1, 49). Members of the major group HRVs bind to the intercellular adhesion molecule 1 (ICAM-1) (15, 44), whereas serotypes of the minor group use various members of the low-density lipoprotein receptor family (18).Upon receptor binding, the viral particle is internalized by receptor-mediated endocytosis. After acidification of the late endosome and subsequent uncoating, the RNA of minor group HRVs is released into the cytoplasm (32). Then the viral RNA is translated into a single large polyprotein from an internal ribosome entry site (IRES), which is located in the 5Ј untranslated region of the HRV genome. The polyprotein is processed into the mature viral proteins through a sequence of cleavages performed by two virus-encoded prot...

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“…37 Synthesis of specific viral macromolecules at an early stage of infection plays a critical role in inducing apoptosis. 104,105 Further, it was apoptotic chorionic cells, not amnion cells, that induced secretion of bioactive IL-6 and TNF-a in vitro. 106 Thus, IAV infection of the fetal chorionic membrane results in a cellular proinflammatory cytokine response with associated apoptosis.…”

Section: Immune Responses At the Maternal-fetal Interfacementioning

confidence: 99%

Influenza, Immune System, and Pregnancy

2014

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Influenza is a major health problem worldwide. Both seasonal influenza and pandemics take a major toll on the health and economy of our country. The present review focuses on the virology and complex immunology of this RNA virus in general and in relation to pregnancy. The goal is to attempt to explain the increased morbidity and mortality seen in infection during pregnancy. We discuss elements of innate and adaptive immunity as well as placental cellular responses to infection. In addition, we delineate findings in animal models as well as human disease. Increased knowledge of maternal and fetal immunologic responses to influenza is needed. However, enhanced understanding of nonimmune, pregnancy-specific factors influencing direct interaction of the virus with host cells is also important for the development of more effective prevention and treatment options in the future.

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Effect of antioxidants on apoptosis induced by influenza virus infection: inhibition of viral gene replication and transcription with pyrrolidine dithiocarbamate

Cited by 94 publications

References 32 publications

Predominant Contribution of IFN-.BETA. Expression to Apoptosis Induction in Human Uterine Cervical Fibroblast Cells by Influenza-Virus Infection

Predominant Contribution of IFN-.BETA. Expression to Apoptosis Induction in Human Uterine Cervical Fibroblast Cells by Influenza-Virus Infection

Inhibition of Polyprotein Processing and RNA Replication of Human Rhinovirus by Pyrrolidine Dithiocarbamate Involves Metal Ions

Influenza, Immune System, and Pregnancy

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