Innate immune evasion by hepatitis C virus and West Nile virus

Antiviral immunity in mammals involves several levels of surveillance and effector actions by host factors to detect viral pathogens, trigger /β interferon production, and to mediate innate defenses within infected cells. Our studies have focused on understanding how these processes are regulated during infection by hepatitis C virus (HCV) and West Nile virus (WNV). Both viruses are members of the Flaviviridae and are human pathogens, but they each mediate a very different disease and course of infection. Our results demonstrate common and unique innate immune interactions of each virus that govern antiviral immunity and demonstrate the central role of /β interferon immune defenses in controlling the outcome of infection.     

流感病毒感染介导的免疫病理损伤研究进展

流感病毒感染(如暴发性流行或高致病性禽流感H5N1感染)可以造成广泛的病理损伤及严重的并发症,其肺部病理损伤以肺水肿及广泛的炎性渗出为特点,并伴有大量的中性粒细胞、巨噬细胞、淋巴细胞浸润及促炎因子和趋化因子的产生．组织学及病理学研究表明,过度的宿主应答反应是介导病理损伤的主要原因之一,而这些在流感病毒感染过程中介导组织损伤的免疫分子与细胞,在病毒的有效清除过程中同样至关重要．主要对甲型流感病毒感染过程中免疫系统的多种效应成分如何引发及加重病理性损伤等有害方面加以综述．为深入了解流感病毒感染防御机制及寻找并设计出既无害又能有效地治疗流感病毒感染的策略提供理论指导．     

T-cell transformation by Marek's disease virus

Marek's disease virus (MDV) is an avian herpesvirus that causes rapid development of T-cell lymphomas in chickens. The MDV genes currently thought to be involved in lymphomagenesis include a bZIP transactivator that is homologous to fos and jun oncogenes but do not appear to have counterparts in other oncogenic herpesviruses.     

Kinetics of virus inactivation by ammonia

Ammonia has been shown to be virucidal in sludge and NH(4)Cl solutions, although the rates at which viruses are inactivated have not been thoroughly studied. In the present studies, the kinetics of the poliovirus type 1 (strain CHAT) and bacteriophage f2 inactivation were examined in such a way that the effects of OH(-) and NH(4) (+) could be separated from those of NH(3). Purified virus stocks were placed into solutions of NH(4)Cl and control solutions containing an equivalent concentration of NaCl and incubated at 20 degrees C. The percentage of virus surviving was calculated, and the kinetics were evaluated by constructing semilogarithmic plots of data. At all pH values and NH(3) concentrations studied, the kinetics of the inactivation of both viruses were pseudo-first order. OH(-) had no measurable effect on the viruses, whereas the effects of NH(4) (+) and Na(+) were similar. A dose-response relationship between NH(3) and the viruses was also found. Bacteriophage f2 was approximately 4.5 times more resistant to the effects of NH(3) than was poliovirus.     

Inhibition of Mengo virus by interferon

Gauntt, Charles J. (The University of Texas, Austin), and Royce Z. Lockart, Jr. Inhibition of Mengo virus by interferon. J. Bacteriol. 91:176-182. 1966.-The inhibition of Mengo virus replication in L cells resulting from interferon was studied quantitatively. Interferon was titrated on L cells with Western equine encephalomyelitis (WEE) virus as the challenge virus. One protective unit (PU) of interferon is the least amount of interferon which prevents cytopathic effects when a large multiplicity of WEE virus is added subsequent to overnight incubation with interferon. Ten PU of interferon reduced the yields of Mengo virus by about 90%. Larger doses of interferon, up to 220 PU, caused no further reduction in the amount of virus produced. Plaque formation by Mengo virus was also reduced in number by about 85 to 90%, but could not be further reduced. The plaques which formed on interferon-treated cells were reduced in size. We were unable to obtain a virus population with increased resistance to interferon action by use of five successive growth cycles in interferon-treated cultures. Analysis of the cell population for the proportion of cells able to act as infectious centers revealed that incubation of cells with 10 PU of interferon decreased the proportion of virus-yielding cells by 80%. The yield of virus per virus-producing cell was decreased by 40 to 60%. Despite the reduction in yields, plaques, and infectious centers resulting from interferon, all doses of interferon failed to prevent the complete destruction of the cells. Experiments with puromycin indicated that the cytopathic effects observed in L cells infected with Mengo virus required that a virus-directed protein be synthesized between 4 and 5 hr postinfection. The evidence suggested, therefore, that the Mengo virus genome was able to code for new protein synthesis in the absence of the production of infectious virus.     

Characterization of virus produced by a lymphoma induced by inoculation of AKR MCF-247 virus.

We report the characterization of the virus produced by a lymphoid cell line derived from a lymphoma of an AKR mouse after injection of the polytropic AKR virus MCF-247. The virus displays polytropic host range properties and is indistinguishable from MCF-247 as judged by analysis of the large RNase T1-resistant oligonucleotides of the RNA genome. Restriction enzyme analysis of cellular DNA revealed the presence of sequences homologous to MCF-247 genomic RNA. The EcoRI cleavage fragments were characteristic of MCF-247 DNA provirus cleavage products.