RNAs of influenza A, B, and C viruses.

The nucleic acids of influenza A, B, and C viruses were compared. Susceptibility to nucleases demonstrates that influenza C virus, just as influenza A and B viruses, possesses single-stranded RNA as its genome. The base compositions of the RNAs of influenza A, B, and influenza C virus are almost identical and comparative analysis on polyacrylamide gels shows that the genome of influenza C/GL/1167/54 virus, like that of the RNAs of influenza A and B viruses, is segmented. Eight distinct RNA bands were found for influenza A/PR/8/34 virus and for influenza B/Lee/40 virus. The RNA of influenza C/GL/1167/54 virus separated into at least four segments. The total molecular weights of the RNA of influenza A/PR/8/34 and B/Lee/40 virus were calculated to be 5.29 X 10(6) and 6.43 X 10(6), respectively. A minimum value of 4.67 X 10(6) daltons was obtained for influenza C/GL/1167/54 virus RNA. The data suggest that influenza C viruses are true members of the influenza virus group.     

Two Loci Controlling Genetic Cellular Resistance to Avian Leukosis-Sarcoma Viruses

Female chickens known to be heterozygous for resistance to subgroups A and B of the avian leukosis-sarcoma viruses were mated to males known to be homozygously resistant to both. The progeny were assayed both on the chorioallantoic membrane (CAM) and in tissue culture for resistance to representative viruses of the A, B, and tentatively defined C subgroups. Segregation ratios of resistance to A and B subgroup viruses agreed with the previously suggested hypothesis of single-autosomal-recessive genes controlling resistance to each subgroup. Mixed infection on the CAM and replicate plate infection in tissue culture with subgroup A and B viruses showed that resistance to the A and B subgroups was inherited independently. Assays with viruses tentatively classified as subgroup C indicated that they were largely composed of a mixture of subgroup A and B viruses or of particles possessing the host range specificity of both. However, virus stocks of the subgroup C category, as well as some stocks classified as subgroup B, produced small numbers of pocks or foci on individuals known to be resistant to subgroup A and B viruses. It is suggested that these Rous sarcoma virus stocks carry between 1 and 10% of a true subgroup C virus.     

Effects of schistosomes on host anti-viral immune response and the acquisition,virulence, and prevention of viral infections: A systematic review

Although a growing number of studies suggest interactions between Schistosoma parasites and viral infections, the effects of schistosome infections on the host response to viruses have not been evaluated comprehensively. In this systematic review, we investigated how schistosomes impact incidence, virulence, and prevention of viral infections in humans and animals. We also evaluated immune effects of schistosomes in those coinfected with viruses. We screened 4,730 studies and included 103. Schistosomes may increase susceptibility to some viruses, including HIV and Kaposi’s sarcoma-associated herpesvirus, and virulence of hepatitis B and C viruses. In contrast, schistosome infection may be protective in chronic HIV, Human T-cell Lymphotropic Virus-Type 1, and respiratory viruses, though further research is needed. Schistosome infections were consistently reported to impair immune responses to hepatitis B and possibly measles vaccines. Understanding the interplay between schistosomes and viruses has ramifications for anti-viral vaccination strategies and global control of viral infections.     

Phenotypic and genotypic comparisons of CCR5- and CXCR4-tropic human immunodeficiency virus type 1 biological clones isolated from subtype C-infected individuals

Individuals infected with human immunodeficiency virus type 1 (HIV-1) subtype C infrequently harbour X4 viruses. We studied R5 and X4 biological clones generated from HIV-1 subtype C-infected individuals. All subtype C R5 viruses demonstrated slower profiles of replication on CD4⁺ lymphocytes in comparison to subtype B viruses, whereas subtype C X4 viruses replicated with comparable efficiency to subtype B X4 viruses. No differences were identified in CC or CXC chemokine inhibitions (RANTES and SDF-1α, respectively) between subtype C and subtype B viruses. Immature dendritic cells were shown in coculture experiments to similarly enhance the infection of subtype C and subtype B R5 as well as X4 viruses. By amino acid sequence analysis, we showed that the R5 and X4 subtype C gp120 envelope gene alterations were similar to those for a switching subtype B virus, specifically with respect to the V3 charge and envelope N-linked glycosylation patterns. By phylogenetic analysis, we showed that one patient was infected with HIV-1 C′ and the other was infected with HIV-1 C" and that one of the patients harbored a virus that was a recombinant in the gp120 env gene between an R5 and an X4 virus, with the resultant virus being R5. No differences were identified between the long terminal repeat regions of the subtype C R5 and X4 biological clones. These results indicate that even though R5 subtype C viruses are restrictive for virus replication, the R5-to-X4 phenotype switch can occur and does so in a manner similar to that of subtype B viruses.     

Virally associated arthritis 2008: clinical,epidemiologic, and pathophysiologic considerations

Several viruses have been associated with the development of inflammatory arthritis, including the hepatitis viruses (hepatitis B virus and hepatitis C virus), HIV, the parvovirus B19, the human T-cell lymphotropic virus-I, and the alphaviruses. Here, we review the epidemiology, the pathophysiological mechanisms, the pertinent clinical and laboratory findings as well as the principles of therapy of the most common virus-associated arthritides. We believe that the knowledge of these key diagnostic and therapeutic features of virus-associated arthritides is important for the rheumatologist of the 21st century.     

A、B、C三型流感病毒病毒学、流行病学、临床特征和流感疫苗

２０世纪人类遭受了４次流感大流行,数千万人失去了生命,流感病毒分Ａ、Ｂ、Ｃ三型,对其病毒学、流行病学和临床特征,以及流感病毒传统疫苗－－灭活疫苗和新型疫苗－－核酸疫苗的研究进展作了论述。     

The DBA.2 mouse is susceptible to disease following infection with a broad, but limited, range of influenza A and B viruses

We assessed the relative susceptibilities to disease of the DBA.2 and C57BL/6 mouse models upon infection with a range of influenza A and B viruses. DBA.2 mice were more susceptible to disease upon inoculation with human H1N1 influenza A virus strains, several swine influenza viruses, and influenza B viruses but were not overtly susceptible to infection with human seasonal H3N2 strains. Hemagglutination inhibition and immunoglobulin isotype profiling indicated that DBA.2 and C57BL/6 mice generate comparable humoral responses upon equivalent 50% mouse lethal dose (MLD(50)) challenges with influenza virus. Our data demonstrate the utility of DBA.2 mice for the elucidation of influenza virus pathogenicity determinants and the testing of influenza vaccines.     

Growth of epizootic hemorrhagic disease, akabane, and ephemeral fever viruses in Aedes albopictus cells maintained at various temperatures

The growth curves of one epizootic hemorrhagic disease (EHD) virus serotype (Reoviridae), two Akabane virus strains (Bunyaviridae) and three bovine ephemeral fever (BEF) group viruses (Rhabdoviridae) were determined in Aedes albopictus cells maintained at 15, 20, 28 and 33 degrees C. Ae albopictus cells supported the growth of all the viruses although not necessarily at all temperatures. Because none of the viruses exhibited cytopathic effect in Ae albopictus cells, growth was assayed in baby hamster kidney 21 (BHK21) cells maintained at 37 degrees C. The temperature at which the Ae albopictus cells were maintained had a marked effect on the growth and yield for each virus studied. EHD virus was heat-stable and grew after 4 days at 28 and 33 degrees C, and after 8 days at 20 degrees C. No growth was recorded up to 12 days at 15 degrees C. The two Akabane viruses were heat-sensitive and exhibited different growth patterns. One strain (B8935) showed no growth at 15 degrees C and only minimal growth at 20, 28 and 33 degrees C. The other strain (CSIRO 16) showed growth after 1-2 days at all temperatures with higher titres reached at 15 and 20 degrees C than at 28 and 33 degrees C. The BEF group viruses grew to approximately the same titres at all temperatures. At the higher temperatures (28 and 33 degrees C) most of BEF group viruses had disappeared within 9 days. In contrast at the lower temperatures (15 and 20 degrees C), there was still virus present 18 days after inoculation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Neuroattenuated bunyavirus variant: derivation, characterization, and revertant clones.

A neuroattenuated variant bunyavirus, designated RFC/25B.5 (B.5), was selected by serial passage of a reassortant clone (RFC virus) of a California serogroup virus in BHK-21 cells, followed by plaque purification of that passaged stock. Based on its virulence index (ratio of PFU/50% lethal dose), clone B5 was over 40,000-fold less virulent than its unpassaged RFC parent after intracerebral (i.c.) inoculation into adult mice. Clone B.5 also exhibited markedly reduced neuroinvasiveness after subcutaneous injection into neonatal mice, although it retained its ability to replicate and kill suckling mice after i.c. injection. A murine neuroblastoma line (NA cells) can be used as an in vitro surrogate for the adult mouse brain, since clone B.5 replicated to at least 1,000-fold-lower titers in NA cells than did several neurovirulent California serogroup viruses. Clone B.5 replicated in BHK-21 cells at 37 degrees C to titers similar to those achieved by other California serogroup viruses but was temperature sensitive (ts) since its replication was markedly restricted at 38.9 degrees C. Ten ts revertant clones of B.5 virus were selected at 38.9 degrees C, and all of them lost their ts phenotype and regained the ability to replicate to high titer in NA cells and to kill adult mice after i.c. injection. Clone B.5 is the first described California serogroup virus which is truly attenuated after i.c. inoculation, and its availability will permit genetic analysis of bunyavirus neurovirulence.     

Influenza viruses as lymphocyte mitogens. I. B cell mitogenesis by influenza A viruses of the H2 and H6 subtypes is controlled by the I-E/C subregion of the major histocompatibility complex

Influenza A viruses of the H2, H3, and H6 subtypes function as T cell-independent B cell mitogens for lymphocytes from BALB/c mice. Lymphocytes from C57BL/10 mice, however, undergo mitogenesis only in response to H3 viruses. The failure of C57BL/10 lymphocytes to respond to H2 and H6 viruses was shown not to reflect a difference in dose-response profile or kinetics of the response, nor was it due to the activity of suppressor T cells. Experiments with congenic and recombinant strains of mice established that mitogenic responsiveness to H2 and H6 viruses is linked to the major histocompatibility complex, and is controlled by a gene located in the I-E/C subregion. Furthermore, responsiveness was shown to correlate with the expression of surface I-E antigen, being positive for mouse strains that express I-E antigen (haplotypes a, d, k, p, r) and negative for strains that do not (haplotypes b, f, q, s). The data suggest that influenza A viruses of the H2 and H6 subtypes may interact directly with I-E molecules on the surface of B cells or possibly on an accessory cell. Because mitogenesis by H3 viruses is not I-E dependent, it appears that influenza A viruses stimulate B cell mitogenesis by at least two different mechanisms.     

Infection of resistant avian cells by subgroup B Rous sarcoma virus.

Chicken fibroblasts derived from the H & N flock, which have been characterized as resistant to subgroup B avian oncornaviruses in focus assays, can be infected in suspension shortly after trypsinization by subgroup B sarcoma and leukosis viruses. Once cells are plated, resistance to infection reappears rapidly. C/BE cell suspensions obtained by treatment with EDTA instead of trypsin are not as sensitive to infection. Late interference established by preinfection with subgroup B leukosis viruses is not overcome by trypsinization. In addition to C/BE H & N chicken cells, C/ABE RPRL line 7 cells can also be infected by subgroup B viruses shortly after trypsinization; however, none of the cell types can be made sensitive to subgroup E infection. These results are discussed in relation to current information on the genetic control of resistance to avian oncornaviruses.     

Hepatitis Viruses and Human Hepatocellular Carcinoma

Two hepatotropic viruses, hepatitis B and C viruses, are known to cause hepatocellular carcinoma in humans. Hepatocarcinogenesis is a complex, stepwise process that evolves over several to many years and precisely how hepatitis viruses contribute to malignant transformation of hepatocytes is uncertain. Hepatitis B vrus is integrated into cellular DNA in the great majority of hepatitis B virus-related hepatocellular carcinomas, whereas replicative intermediates of hepatitis C virus do not insert into chromosomal DNA, making it likely that different pathogenetic mechanisms operate with the two viruses. Indeed, evidence is mounting that both direct and indirect carcinogenic mechanisms, and often the two together, are involved in virus-induced hepatocellular carcinoma. In addition, evidence is now available that hepatitis B and C viruses interact synergistically in the pathogenesis of hepatocellular carcinoma. Animal models, — other members of the Hepadnaviridae family that cause tumors in their respecitve animal hosts, and transgenic mice into which the sequences of hepatitis B virus DNA have been inserted — are proving useful in elucidating putative mechanisms of hepatitis B virus-related hepatocarcinogenesis. Whatever the genesis of hepatitis virus-induced hepatocellular carcinoma, it is clear that hepatitis viruses do not act alone but in conjunction with other environmental carcinogens and a number of host factors.     

VIRUS DISEASES OF CACAO IN WEST AFRICAL: II. CROSS-IMMUNITY EXPERIMENTS WITH VIRUSES 1A, 1B AND 1C

Experiments on cross-immunity reactions between three viruses attacking Theobroma cacao L. on the Gold Coast are described. A field trial involving 3 acres of graft-inoculated trees revealed some degree of protection afforded by Theobroma virus 1B against infection with virus 1A. The protection appeared to be more effective against insect inoculation than against graft transmission, being only temporary in the latter. Virus 1C (probably unrelated but not to be called Theobroma virus 2 until more evidence is available) conferred no protection against virus 1A.
The latent periods for these viruses were calculated from this experiment, which also provided data on their effects on yield. Virus 1A reduced yield by 50% in the first year after inoculation and killed the trees in the second. Virus 1B had no appreciable effect on yield; virus 1C reduced yield by 50 % in the third year after inoculation but there was no further decline in the fourth.
The rates of spread of these viruses were compared and significant differences demonstrated.     

利用寡核苷酸微阵列技术对HBV、HCV、HIV、HAV、GBV-C/HGV和B19进行同时监测的初步研究

探讨研制能同时检测HBV、HCV、HIV、HAV、GBV-C/HGV和B19的微阵列监控芯片。根据病毒公开发表序列,序列比对,得出保守区域,设计病毒的特异性检测探针,同时设置阴性、阳性参照探针,制备监控微阵列。利用随机引物PCR方法标记样品中的病毒靶序列,标记产物与微阵列上的探针杂交,清洗、扫描后进行结果分析。通过对质粒或模式分子的检测以及经HBV、HCV、HIV临床标本的验证,发现该微阵列监控芯片具有良好的特异性。其对质粒的检测灵敏度可达102病毒拷贝数,对临床标本的检测灵敏度可达103病毒拷贝数。此外,该微阵列监控芯片可检测出病毒混合感染血清。为微阵列监控芯片应用于此六种血液病毒的检测打下一定的基础。     

Hepatitis B,Hepatitis C and HIV-1 Coinfection in Two Informal Urban Settlements in Nairobi,Kenya

Background

HIV-1 and Hepatitis B and C viruses coinfection is common in Sub-Saharan Africa due to similar routes of transmission and high levels of poverty. Most studies on HIV-1 and Hepatitis B and C viruses have occurred in hospital settings and blood transfusion units. Data on Hepatitis B and C viruses and HIV-1 coinfection in informal urban settlements in Kenya are scanty, yet they could partly explain the disproportionately high morbidity and mortality associated with HIV-1 infections in these slums.

Objectives

The objective of this study was to determine the prevalence of HIV and Hepatitis B and C dual infection in urban slums in Nairobi.

Methods

Blood samples were collected from residents of Viwandani and Korogocho between 2006 and 2007. A structured questionnaire was used to obtain socio-demographic data from participants. Samples were screened for Hepatitis B surface antigen (HBsAg), anti-HCV and anti-HIV-1. Statistical analysis was done using STATA.

Results

Samples were successfully collected from 418 (32%) men and 890 (68%) females. The HIV-1, HBV and HCV prevalence was 20.4%, 13.3% and 0.76% respectively at the time of the study. Of the 268 (20.4%) HIV-1 positive participants, 56 (4.26%) had HBV while 6 (0.46%) had HCV. Of the 1041 HIV-1 negative participants, 117 (8.9%) had HBV while 4 (0.31%) had HCV. Only two people (0.15%) were co-infected with all the three viruses together.

Discussion

The odds of getting hepatitis infection were higher in HIV-1 participants (for HBV OR 2.08,p<0.005 and for HCV OR 5.93, p<0.005). HIV prevalence rates were similar in both informal settlements. HIV infection was highest in age group 35-39 years and among the divorced/separated or widowed. Prevalence of all viruses was highest in those who did not have any formal education.

Conclusion

The HIV prevalence in these informal settlements suggests a higher rate than what is observed nationally. The prevalence rates of HBV are significantly higher in the HIV-1 positive and negative populations. HCV as well as triple HIV-1, HBV and HCV coinfection are uncommon in Korogocho and Viwandani. This clearly indicates the need for HIV-1 control programmes and hepatitis B virus vaccination to be promoted through public awareness as preventive strategy.     

Seroprevalence of the Hepatitis B,Hepatitis C,and Human Immunodeficiency Viruses and Treponema pallidum at the Beijing General Hospital from 2010 to 2014: A Cross-Sectional Study

BackgroundThe hepatitis B, hepatitis C, human immunodeficiency viruses and Treponema pallidum are important causes of infectious diseases concern to public health.MethodsBetween 2010 and 2014, we used an automated chemiluminescence microparticle immunoassay to detect the hepatitis B, hepatitis C, and human immunodeficiency viruses as well as Treponema pallidum (the rapid plasma regain test was used in 2010–2011). Positive human immunodeficiency virus tests were confirmed via western blotting.ResultsAmong 416,130 subjects, the seroprevalences for hepatitis B virus, hepatitis C virus, human immunodeficiency virus, and Treponema pallidum were 5.72%, 1.23%, 0.196%, and 0.76%, respectively. Among 671 patients with positive human immunodeficiency virus results, 392 cases were confirmed via western blotting. Hepatitis B and human immunodeficiency virus infections were more frequent in men (7.78% and 0.26%, respectively) than in women (4.45% and 0.021%, respectively). The hepatitis B and C virus seroprevalences decreased from 6.21% and 1.58%, respectively, in 2010, to 5.37% and 0.988%, respectively, in 2014. The human immunodeficiency virus seroprevalence increased from 0.04% in 2010 to 0.17% in 2014, and was elevated in the Infectious Disease (2.65%), Emergency (1.71%), and Dermatology and Sexually Transmitted Diseases (1.12%) departments. The specificity of the human immunodeficiency virus screening was 71.4%. The false positive rates for the Treponema pallidum screening tests increased in patients who were 60–70 years old. The co-infection rates for the hepatitis C and human immunodeficiency viruses were 0.47% in hepatitis C virus-positive patients and 7.33% in human immunodeficiency virus-positive patients.ConclusionsDuring 2010–2014, hepatitis B virus and human immunodeficiency virus infections were more frequent among men at our institution. Although the seroprevalences of hepatitis B and C viruses decreased, the seroprevalence of human immunodeficiency virus infection increased (with higher seroprevalences in high-risk departments). Older patients were more likely to exhibit false positive findings for syphilis.     

A human immunodeficiency virus prime-boost immunization regimen in humans induces antibodies that show interclade cross-reactivity and neutralize several X4-, R5-, and dualtropic clade B and C primary isolates

A human immunodeficiency virus (HIV) vaccine that will be useful in diverse geographic regions will need to induce a broad immune response characterized by cross-clade immunity. To test whether a clade B-based HIV candidate vaccine could induce interclade humoral responses, including neutralizing activity against primary HIV-1 isolates, sera were tested from recipients of a vaccine consisting of recombinant canarypox virus vCP205 and recombinant gp120(SF2). Serum antibodies exhibited strong immunochemical cross-reactivity with V3 peptides from clades B, C, and F, with weaker activity for several V3 peptides from clades A, D, G, and H; essentially no reactivity could be demonstrated with V3 peptides from clades E and O. Extensive cross-clade reactivity was also documented by enzyme-linked immunosorbent assay with all nine recombinant HIV envelope glycoproteins tested from clades B, D, and E. In addition, vaccinees' sera displayed significant neutralizing activity against 5 of 14 primary isolates tested, including one X4 virus and two dualtropic viruses (from clade B) and two R5 viruses (from clades B and C). This is the first demonstration of the induction by a candidate HIV vaccine constructed from clade B laboratory strains of HIV of neutralizing activity against R5 and clade C primary isolates. The data suggest that, by virtue of their ability to induce cross-clade immune responses, appropriately formulated HIV vaccines based on a finite number of HIV isolates may ultimately be able to protect against the wide range of HIV isolates affecting the populations of many geographic regions.     

HIV infection in India: Epidemiology, molecular epidemiology and pathogenesis

The year 1986 saw first case of HIV infection as well as first report of AIDS case in India. Since then the epidemic has spread throughout the country. In the recent years there is evidence of epidemic being stabilized with decrease in new infections reported from some parts of the country. The absolute number of HIV infections in the country is expected to be close to 2.5 million and National AIDS Control Programme, phase III is geared to contain the epidemic. HIV viruses circulating in India predominantly belong to HIV-1 subtype C. However, there have been occasional reports of HIV-1 subtype A and B. Matter of concern is reports of A/C and B/C mosaic viruses that are being reported from different parts of the country. The data on HIV drug resistance from India is rather limited. Most of the studies have shown that the virus strains from drug naïve patients do not show significant level of drug resistance mutations. The few immunological studies in Indian patients show that the Indian HIV infected patients show both HIV-specific CTL responses as well as neutralizing antibody response. Mapping of CTL epitopes showed that while Indian patients identify same regions of Gag antigen as recognized by South African subtype C infected patients, some regions are uniquely recognized by Indian patients. There are very few studies on host genetic factors in India in context with HIV infection. However there are evidences reported of association of host genetic factors such as HLA types and haplotypes and HIV disease.     

Biochemical analysis of the p30''s of N-, B-, and B leads to NB-tropic murine leukemia viruses of BALB/c origin.

Previous analysis of the virion proteins of an N- and a B-tropic type C virus of BALB/c mice, of 16 N-tropic recombinants (XLPN viruses) between these viruses, and of eight NB-tropic viruses derived from the B-tropic virus suggested that among these closely related viruses N-, B-, or NB-tropism was associated with the electrophoretic mobility of p30 on sodium dodecyl sulfate-polyacrylamide gels, and thus that p30 might determine this phenotype. To obtain further evidence for the association of structural markers of p30 with N-, B-, or NB-tropism, we have analyzed the p30's of these same viruses by using two-dimensional tryptic peptide mapping and slab gel isoelectric focusing. The results of these analyses suggest that (i) a single peptide unique to the N-tropic virus p30- is present in the p30 of all N-tropic recombinants; (ii) a single peptide unique to the B virus p30 is not present in p30's of the N-tropic recombinants, and this peptide is also absent in p30's of NB-tropic viruses derived from the B-tropic virus; and (iii) p30's of NB-tropic viruses possess a new tryptic peptide not found in the p30 of their B-tropic virus progenitors, and this new peptide is not found in the p30 of the N-tropic virus of BALB/c or the XLPN viruses. These results are consistent with the possibility that p30 may determine the N-, B-, or NB-tropism of murine leukemia viruses. In addition, these studies indicate that some of the N-tropic recombinants have experienced recombination within the p30 gene.     

Zamilon,a Novel Virophage with Mimiviridae Host Specificity

Virophages, which are potentially important ecological regulators, have been discovered in association with members of the order Megavirales. Sputnik virophages target the Mimiviridae, Mavirus was identified with the Cafeteria roenbergensis virus, and virophage genomes reconstructed by metagenomic analyses may be associated with the Phycodnaviridae. Despite the fact that the Sputnik virophages were isolated with viruses belonging to group A of the Mimiviridae, they can grow in amoebae infected by Mimiviridae from groups A, B or C. In this study we describe Zamilon, the first virophage isolated with a member of group C of the Mimiviridae family. By co-culturing amoebae with purified Zamilon, we found that the virophage is able to multiply with members of groups B and C of the Mimiviridae family but not with viruses from group A. Zamilon has a 17,276 bp DNA genome that potentially encodes 20 genes. Most of these genes are closely related to genes from the Sputnik virophage, yet two are more related to Megavirus chiliensis genes, a group B Mimiviridae, and one to Moumouvirus monve transpoviron.