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Virus Titre (virus + titre)
Selected AbstractsAnti-influenza virus activity of crude extract of Ribes nigrum L.PHYTOTHERAPY RESEARCH, Issue 2 2003Yoko M. Knox Abstract This experiment was designed to detect the antiviral activities of crude fruit extracts of wild Ribes nigrum L. (Kurokarin extract) against influenza virus types A and B. Kurokarin extract was prepared as follows: fruits of Ribes nigrum L. were heated at 50,°C in a heating tank, and then ground under anaerobic conditions. The extracts were centrifuged, and the supernatant fluid was filtered and sterilized by infrared rays. The crude extract was diluted with Eagle's minimum essential medium (MEM) and the solution was adjusted to a pH 7.2 with 0.1 N or 1 N NaOH. Proven anti-influenza virus effects of the extracts were shown. The concentration of extract required to inhibit the plaque formation of both IVA and IVB by 50% (IC50) was 3.2,,g/mL. Both IVA and IVB were directly inactivated up to 99% by 10,,g/mL of the extract at pH 2.8, and 95% to 98% by this dose at pH 7.2. The growth of IVA in cells treated with 10 and 100,,g/mL of the extract for 6,h after infection was completely suppressed. Virus titres in culture fluids of the cells treated with 100,,g/mL of Kurokarin extract for 1,h at 8 to 9,h after infection, were completely suppressed, indicating that the extract inhibited the virus release from the infected cells. Copyright © 2003 John Wiley & Sons, Ltd. [source] The lack of RNA-dependent protein kinase enhances susceptibility of mice to genital herpes simplex virus type 2 infectionIMMUNOLOGY, Issue 4 2006Daniel J. J. Carr Summary Mice deficient in RNA-dependent protein kinase (PKR,/,) or deficient in PKR and a functional 2,,5,-oligoadenylate synthetase (OAS) pathway (PKR/RL,/,) are more susceptible to genital herpes simplex virus type 2 (HSV-2) infection than wild-type mice or mice that are deficient only in a functional OAS pathway (RL,/,) as measured by survival over 30 days. The increase in susceptibility correlated with an increase in virus titre recovered from vaginal tissue or brainstem of infected mice during acute infection. There was also an increase in CD45+ cells and CD8+ T cells residing in the central nervous system of HSV-2-infected PKR/RL,/, mice in comparison with RL,/, or wild-type control animals. In contrast, there was a reduction in the HSV-specific CD8+ T cells within the draining lymph node of the PKR/RL,/, mice. Collectively, activation of PKR, but not of OAS, contributes significantly to the local control and spread of HSV-2 following genital infection. [source] Neutralization kinetics of sensitive and resistant subtype B primary human immunodeficiency virus type 1 isolatesJOURNAL OF MEDICAL VIROLOGY, Issue 7 2006David Davis Abstract The aim of the study was to determine if sensitive and resistant human immunodeficiency virus type 1 (HIV-1) subtype B primary isolates have different neutralization kinetics. Neutralization assays were undertaken where either the time allowed for virus to react with antibodies or the subsequent period of this mixture's exposure to target cells were varied. The relative neutralization sensitivity/resistance is a reproducible property of the isolates. In a minority of combinations, the titre falls exponentially for as long as the free virions are exposed to antibody. In the remainder, neutralization kinetics shows deviations which may be attributed to events occurring after the virus,antibody mixture is added to the target cells: significant neutralization with minimal exposure of the free virions to antibody; a plot where reduction in virus titre is parallel to the duration of the incubation phase of the assay. Neutralization rate constants are similar for primary HIV-1 SF33, HIV-1 SF162, and HIV-1 89.6, reaching 5,×,105,1,×,106/M sec for the monoclonal antibody IgG1 b12. However, although increased antibody levels produced greater reductions in virus titre the rate of neutralization was not proportional to the antibody concentration. Neutralization of either the free virion or cell-associated virus does not correlate with the resistance/sensitivity of primary subtype B isolates. The target cells play an active role, so that in designing neutralization assays with primary isolates of HIV-1, events following the virus,antibody complex binding to the cell surface have to be taken into consideration. J. Med. Virol. 78:864,876, 2006. © 2006 Wiley-Liss, Inc. [source] Oral susceptibility of South African Culicoides species to live-attenuated serotype-specific vaccine strains of African horse sickness virus (AHSV)MEDICAL AND VETERINARY ENTOMOLOGY, Issue 4 2003J. T. Paweska Abstract., The oral susceptibility of livestock-associated South African Culicoides midges (Diptera: Ceratopogonidae) to infection with the tissue culture-attenuated vaccine strains of African horse sickness virus (AHSV) currently in use is reported. Field-collected Culicoides were fed on horse blood-virus mixtures each containing one of the seven serotype-specific vaccine strains of AHSV, namely serotypes 1, 2, 3, 4, 6, 7 and 8. The mean titres of virus in the bloodmeals for the seven vaccine strains were between 6.8 and 7.6 log10TCID50/mL. All females (n = 3262) that survived 10 days extrinsic incubation (10 dEI) at 23.5°C were individually assayed in microplate BHK-21 cell cultures. In midges tested immediately after feeding, AHSV was detected in 96.1% individuals; mean virus titre was 2.0 log10TCID50/midge. After 10 dEI virus recovery rates varied in Culicoides (Avaritia) imicola Kieffer from 1% (AHSV-2) to 11% (AHSV-7) and in Culicoides (A.) bolitinos Meiswinkel from 0% (AHSV-3) to 14.6% (AHSV-2). Although our results indicate that two major field vectors C. imicola and C. bolitinos are susceptible to oral infection with vaccine strains of AHSV, the level of viral replication for most of the vaccine strains tested was below the postulated threshold (=2.5 log10TCID50/midge) for fully disseminated orbivirus infection. In this study, for the first time AHSV has been recovered after 10 dEI from six non- Avaritia livestock-associated Old World species: C. engubandei de Meillon (AHSV-4), C. magnus Colaço (AHSV-3, -4), C. zuluensis de Meillon (AHSV-2, -4), C. pycnostictus Ingram & Macfie (AHSV-2), C. bedfordi Ingram & Macfie (AHSV-7), and C. dutoiti de Meillon (AHSV-7). As little is known about the virogenesis of AHSV in the southern African species of Culicoides, the epidemiological significance of our findings in relation to the potential for transmission of current AHSV vaccine strains by Culicoides requires further assessment. [source] Variation in virus populations and growth characteristics of two sugarcane cultivars naturally infected by Sugarcane yellow leaf virus in different geographical locationsPLANT PATHOLOGY, Issue 5 2007Y. Abu Ahmad Two sugarcane cultivars (R570 and SP71-6163) naturally infected by Sugarcane yellow leaf virus (SCYLV) were each imported from several geographical locations into a sugarcane yellow leaf-free environment (Montpellier, France). Plants were grown as plant cane for 5,6 months and the experiment was repeated for three consecutive years (2003,2005) in a greenhouse. Several sugarcane-growth and disease characteristics were monitored to identify variation in pathogenicity of SCYLV. Depending on their geographical origin, sugarcane cvs R570 and SP71-6163 were infected by SCYLV genotypes BRA-PER or REU, or a mixture of the two. Severity of symptoms did not vary between plants of cv. R570, but variation in disease severity between plants of cv. SP71-6163 from different geographical locations suggested the occurrence of pathogenic variants of SCYLV. For each sugarcane cultivar, differences in stalk length, number of stalk internodes, virus titre in the top visible dewlap leaf, and percentage of infection of leaf and stalk phloem vessels were also found between plants from different geographical origins. However, these differences were not always reproducible from one year to another, suggesting occurrence of different plant responses to SCYLV isolates under varying environmental conditions. [source] Synergism between plant viruses: a mathematical analysis of the epidemiological implicationsPLANT PATHOLOGY, Issue 6 2001X.-S. Zhang Many virus diseases of plants are caused by a synergistic interaction between viruses within the host plant. Such synergism can induce symptoms more severe than would be caused by additive effects. In a synergistic interaction, the virus titre of both, one, or neither virus may be enhanced and, as a consequence, the rate of disease spread may be affected. An epidemiological model was developed in which transmission and loss rates were attributed to the different virus infection possibilities. Sharing the same host population implies competition, and this imposes an increased constraint on the survival of both viruses. It was shown that, in order to ensure virus survival in a mixed infection, the basic reproductive number should exceed a critical value which is larger than unity (R0 > Rc > 1). Here R0 is used in the same sense as in the absence of superinfection. Increased virulence (equivalent to disease severity) in dually infected plants decreases the opportunities for both viruses to coexist, while increased virus transmission from dually infected plants increases such opportunities. The net effect of increased virulence and increased virus transmission on virus persistence was neutral if synergism caused the same proportional effect on both. Total host abundance was, however, reduced. The opportunity for virus persistence was increased if the enhancement of transmission exceeded that of virulence. Indeed, by this mechanism a virus which was nonviable alone could invade and persist in a chronic epidemic of another virus. Where the effect on virulence is greater than that on transmission, the viruses are likely to exclude each other, especially when the transmission rates of both viruses have intermediate values. In such cases, the final outcome is determined by both the parameter values and the initial state. [source] Oral administration of lactobacilli from human intestinal tract protects mice against influenza virus infectionLETTERS IN APPLIED MICROBIOLOGY, Issue 1 2010M. Kawase Abstract Aims:, Our study was conducted to evaluate the potent protective effects of oral administration of probiotic Lactobacillus strains against influenza virus (Flu) infection in a mouse model. Method and Results:, Lyophilized Lactobacillus rhamnosus GG (LGG) and Lactobacillus gasseri TMC0356 (TMC0356) were orally administered to BALB/c mice for 19 days. The test mice were intranasally infected with Flu A/PR/8/34 (H1N1) on day 14, and any changes in clinical symptoms were monitored. After 6 days of infection, the mice were killed and pulmonary virus titres were determined. The clinical symptom scores of mice administered oral LGG and TMC0356 were significantly ameliorated, compared to those of the control mice (P < 0·01). The pulmonary virus titres of the mice fed LGG and TMC0356 were also significantly decreased compared to those of control mice (P < 0·05). Conclusions:, These results indicate that oral administration of lactobacilli, such as LGG and TMC0356, might protect a host animal against Flu infection. Significance and Impact of the Study:, These results demonstrate that oral administration of selected lactobacilli might protect host animals from Flu infection by interactions with gut immunity. [source] Experimental studies of the role of the little raven (Corvus mellori) in surveillance for West Nile virus in AustraliaAUSTRALIAN VETERINARY JOURNAL, Issue 6 2010J Bingham Objective To study the potential role of an Australian corvid, the little raven (Corvus mellori), in the surveillance for exotic West Nile virus (WNV) in Australia. Method In a series of trials, little ravens were infected with WNV (strain 4132 New York 1999) and Kunjin virus (strain K42886) by the intramuscular route. They were observed for 20 days during which blood and swab samples were taken for virus isolation. Tissue samples were taken from ravens humanely killed during the acute infection period, and at the termination of the trials, for virus isolation, histopathology and immunohistochemistry. Results Ravens infected with WNV became mildly ill, but all recovered and seroconverted. Blood virus titres peaked around 3 to 4 days after inoculation at levels between 103.0 to 107.5 plaque forming units/mL. Virus or viral antigen was detected in spleen, liver, lung, kidney, intestine, testis and ovary by virus isolation and/or immunohistochemistry. WNV was detected in oral and cloacal swabs from 2 to 7 days post inoculation. The molecular and pathogenic characteristics of the inocula were consistent with them being of high virulence, as expected for this isolate. Ravens infected with Kunjin virus developed viraemia and seroconverted, although they did not develop disease. Conclusions Little ravens do not develop severe disease in response to virulent WNV infection and for this reason may not be important sentinel hosts in the event of an outbreak of WNV, as in North America. However, as they have relatively high viraemias, they may be able to support virus cycles. 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