Production Of Antiviral Factors Research Articles

Vitamin D treatment of peripheral blood mononuclear cells modulated immune activation and reduced susceptibility to HIV-1 infection of CD4+ T lymphocytes.

IntroductionMucosal immune activation, in the context of sexual transmission of HIV-1 infection, is crucial, as the increased presence of activated T cells enhance susceptibility to infection. In this regard, it has been proposed that immunomodulatory compounds capable of modulating immune activation, such as Vitamin D (VitD) may reduce HIV-1 transmission and might be used as a safe and cost-effective strategy for prevention. Considering this, we examined the in vitro effect of the treatment of peripheral blood mononuclear cells (PBMCs) with the active form of VitD, calcitriol, on cellular activation, function and susceptibility of CD4+ T cells to HIV-1 infection.MethodsWe treated PBMCs from healthy HIV unexposed individuals (Co-HC) and frequently exposed, HIV-1 seronegative individuals (HESNs) from Colombia and from healthy non-exposed individuals from Canada (Ca-HC) with calcitriol and performed in vitro HIV-1 infection assays using X4- and R5-tropic HIV-1 strains respectively. In addition, we evaluated the activation and function of T cells and the expression of viral co-receptors, and select antiviral genes following calcitriol treatment.ResultsCalcitriol reduced the frequency of infected CD4+ T cells and the number of viral particles per cell, for both, X4- and R5-tropic viruses tested in the Co-HC and the Ca-HC, respectively, but not in HESNs. Furthermore, in the Co-HC, calcitriol reduced the frequency of polyclonally activated T cells expressing the activation markers HLA-DR and CD38, and those HLA-DR+CD38-, whereas increased the subpopulation HLA-DR-CD38+. Calcitriol treatment also decreased production of granzyme, IL-2 and MIP-1β by T cells and increased the transcriptional expression of the inhibitor of NF-kB and the antiviral genes cathelicidin (CAMP) and APOBEC3G in PBMCs from Co-HC.ConclusionOur in vitro findings suggest that VitD treatment could reduce HIV-1 transmission through a specific modulation of the activation levels and function of T cells, and the production of antiviral factors. In conclusion, VitD remains as an interesting potential strategy to prevent HIV-1 transmission that should be further explored.

Regulation of the Host Antiviral State by Intercellular Communications.

Viruses usually induce a profound remodeling of host cells, including the usurpation of host machinery to support their replication and production of virions to invade new cells. Nonetheless, recognition of viruses by the host often triggers innate immune signaling, preventing viral spread and modulating the function of immune cells. It conventionally occurs through production of antiviral factors and cytokines by infected cells. Virtually all viruses have evolved mechanisms to blunt such responses. Importantly, it is becoming increasingly recognized that infected cells also transmit signals to regulate innate immunity in uninfected neighboring cells. These alternative pathways are notably mediated by vesicular secretion of various virus- and host-derived products (miRNAs, RNAs, and proteins) and non-infectious viral particles. In this review, we focus on these newly-described modes of cell-to-cell communications and their impact on neighboring cell functions. The reception of these signals can have anti- and pro-viral impacts, as well as more complex effects in the host such as oncogenesis and inflammation. Therefore, these “broadcasting” functions, which might be tuned by an arms race involving selective evolution driven by either the host or the virus, constitute novel and original regulations of viral infection, either highly localized or systemic.

War Archives: How Some Primates Fought Off Ancient Viruses

War Archives: How Some Primates Fought Off Ancient Viruses

Effect of HIV on production of anti-viral factors by HIV-specific CD4+ T cells

Results The CD4+ T cells produced IFN-y and MIP-1a in response to gp120. Also detected were RANTES and MIP-1a, but not MDC (CCL22). The b-chemokines displayed potent inhibitory activities against R5-tropic HIV-1. After the cells were exposed to BX08 (an R5 subtype B HIV-1 primary isolate), the capacity of these cells to produce IFN-y and MIP-1a in response to gp120 was initially comparable with that of the unexposed control. But after 3–4 days of infection, the numbers of cells capable of producing IFNy and MIP-1a decreased significantly, while the percentage of infected cells reached >80%. Conclusion HIV-specific CD4+ T cells are susceptible to HIV. HIV reduces the capacity of the cells to produce IFN-y and bchemokines. On-going efforts to enhance HIV-specific CD4+ T cell resistance against the virus will be presented. from 2006 International Meeting of The Institute of Human Virology Baltimore, USA. 17–21 November, 2006

Production of antiviral factor by infected chick embryonic fibroblasts

Production of antiviral factor by infected chick embryonic fibroblasts

Combined action of salts of heavy metals and phenol on energy metabolism of isolated rat liver mitochondria

The secretion of antiviral factor (AF) by infected cell cultures was examined. Activity of AF depended on the cell culture used. AF produced by infected chick embryo fibroblasts had maximal activity. No activity was registered in BHK-21 cells, whereas human embryo fibroblasts and cell line Vero produced a low level of activity. Actinomycin D and cycloheximide prevented the production of AF. The results indicate that VEE virus-infected chick embryo fibroblasts produce AF which may be attributed to nonspecific factors of cell defense.

Dietary fat affects immune response, production of antiviral factors, and immune complex disease in NZB/NZW mice.

Autoimmune-prone (NZB x NZW)F1 (B/W) mice fed three nearly isocaloric diets with varied fat content showed a marked difference in their spontaneous development of immune complex disease and their immune response. Those animals received the diets high in either unsaturated or saturated fats had more severe immune complex nephritis and died earlier than mice on the low-fat diet. Endogenous production of the mouse xenotropic virus was unaffected by dietary fats, but the serum lipoproteins associated with antiviral activity were increased to levels as high as 1:600,000 in the B/W mice on the high-fat diets. These lipoproteins may be partially responsible for the decreased mitogenic response of spleen cells from mice fed the two high-fat diets. The mice receiving a diet high in saturated fats produced substantially higher titers of natural thymocytotoxic autoantibody, an IgM class of antibody, than did the mice maintained either on the high-unsaturated-fat or low-fat diet. In contrast, the mice receiving the diet high in unsaturated fats made significantly greater levels of antibodies to double-stranded DNA, an IgG, than did the mice kept on the two other diets. These results suggest that the type of fat in the diet could affect the serum level of different immunoglobulin classes. The data provide further evidence that the amount of dietary lipids alone can influence cellular and humoral immune responses and the spontaneous development of immune complex disease.

Further studies on the biology of an antiviral factor (AVF) from virus-infected plants and its association with the N-gene of Nicotiana species.

The antiviral factor (AVF) from virus-infected plants, purified on polyacrylamide gels, could be labelled with radioactive phosphorus and its activity could be eluted from the gels. The radioactivity and the antiviral activity were co-purified and thus co-electrophoresed; hence, the previously reported radioactive zone (Antignus, Sela & Harpaz, 1975) can be regarded as AVF. The production of AVF requires both the presence of the N-gene in the plant as well as virus infection. AVF production is inhibited by actinomycin D, but its activity is not affected by this drug. AVF production is correlated in time with the development of virus resistance in a local-lesion host. AVF inhibits TMV multiplication in infected leaves and suppresses virus synthesis almost totally in a local-lesion host. Some AVF is also produced when Nicotiana glutinosa L. is infected with a non-localized virus, but to a much lesser extent and at a later stage of infection. The production of AVF in N. glutinosa is not blocked at 30 degrees C. even though TMV is no longer localized at this temperature.