The NF-B signaling pathway has previously been shown to be required for efficient influenza A virus replication, although the molecular mechanism is not well understood. In this study, we identified a specific step of the influenza virus life cycle that is influenced by NF-B signaling by using two known NF-B inhibitors and a variety of influenza virus-specific assays. The results of time course experiments suggest that the NF-B inhibitors Bay11-7082 and ammonium pyrrolidinedithiocarbamate inhibited an early postentry step of viral infection, but they did not appear to affect the nucleocytoplasmic trafficking of the viral ribonucleoprotein complex. Instead, we found that the levels of influenza virus genomic RNA (vRNA), but not the corresponding cRNA or mRNA, were specifically reduced by the inhibitors in virus-infected cells, indicating that NF-B signaling is intimately involved in the vRNA synthesis. Furthermore, we showed that the NF-B inhibitors specifically diminished influenza virus RNA transcription from the cRNA promoter but not from the vRNA promoter in a reporter assay, a result which is consistent with data obtained from virus-infected cells. The overexpression of the p65 NF-B molecule could not only eliminate the inhibition but also activate influenza virus RNA transcription from the cRNA promoter. Finally, using p65-specific small interfering RNA, we have shown that p65 knockdown reduced the levels of influenza virus replication and vRNA synthesis. In summary, we have provided evidence showing, for the first time, that the NF-B host signaling pathway can differentially regulate influenza virus RNA synthesis, which may also offer some new perspectives into understanding the host regulation of RNA synthesis by other RNA viruses.

The study was intended to investigate the feasibility of reverse transcription-PCR (RT-PCR) for evaluation of the efficacy of inactivation of viruses in water and to elucidate the mechanisms of inactivation of hepatitis A virus (HAV) by chlorine. Cell culture, enzyme-linked immunosorbent assay, and long-overlap RT-PCR were used to detect the infectivity, antigenicity, and entire genome of HAV inactivated or destroyed by chlorine. The cell culture results revealed the complete inactivation of infectivity after 30 min of exposure to 10 or 20 mg of chlorine per liter and the highest level of sensitivity in the 5 nontranslated regions (5NTR), inactivation of which took as much time as the inactivation of infectivity of HAV by chlorine. However, antigenicity was not completely destroyed under these conditions. Some fractions in the coding region were resistant to chlorine. To determine the specific region of the 5NTR lost, three segments of primers were redesigned to monitor the region from bp 1 to 1023 across the entire genome. It was shown that the sequence from bp 1 to 671 was the region most sensitive to chlorine. The results suggested that the inactivation of HAV by chlorine was due to the loss of the 5NTR. It is believed that PCR can be used to assess the efficacy of disinfection of HAV by chlorine as well as to research the mechanisms of inactivation of viruses by disinfectants.Hepatitis A virus (HAV) is a positive-strand RNA virus that belongs to the Hepatovirus group of the family Picornaviridae, which can bring about infectious hepatitis (hepatitis A). The infection rate of HAV is universally very high, being about 70% in China (18), and person-to-person spread of HAV is also very common. Disinfection with chlorine has been adopted worldwide to ensure the safety of drinking water, since HAV spreads mainly through drinking water and food. However, research on the mechanisms of chlorine inactivation of HAV has been inadequate. It is generally believed that chlorine inactivates HAV by damaging the nucleic acid of the virus (2,3,12). With the development of molecular biology methods, nucleic acid probes and PCR have been used to evaluate the effects of virus disinfection and to research disinfection mechanisms. However, the research problem most frequently encountered and difficult to solve is that, after disinfection, the virus nucleic acid can still be detected by PCR, although the infectivity of the virus actually no longer exists. Therefore, it is generally believed that molecular biology methods cannot be used to evaluate either the effects or the mechanisms of disinfection (2,8,9,16).The assumption that chlorine acts on the virus nucleic acid is likely to be measured by PCR. The main reason why no ideal result has ever been obtained in previous studies is that the length of the virus nucleic acid segment detected is limited and fails to reflect the overall status of viral nucleic acid. So in this study, in addition to using such techniques as cell culture and enzyme-linked immunosorbent assay (ELISA) to d...

This study investigated the long-term excretion of severe acute respiratory syndrome–associated coronavirus in sputum and stool specimens from 56 infected patients. The median (range) duration of virus excretion in sputa and stools was 21 (14–52) and 27 (16–126) days, respectively. Coexisting illness or conditions were associated with longer viral excretion in stools.

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We aimed to evaluate the effectiveness of a family-based intervention program for Internet addiction in Chinese adolescents. Adolescents (N = 57), diagnosed as having Internet addiction, were divided randomly into an intervention group (n = 28) and a control group (n = 29). Participants in the intervention group participated in a 14-session family-based group intervention while participants in the control group received conventional group therapy only. Assessment tools were administered to both groups at baseline, immediately after the intervention, and at 1-month and 3-month follow-ups. Results indicted that the family-based group intervention is more effective in decreasing Internet use and enhancing family function.