Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A polyherbal cream (Basant) has been formulated using diferuloylmethane (curcumin), purified extracts of Emblica officinalis (Amla), purified saponins from Sapindus mukorossi, Aloe vera and rose water along with pharmacopoeially approved excipients and preservatives. Basant inhibits the growth of WHO strains and clinical isolates of Neisseria gonorrhoeae, including those resistant to penicillin, tetracycline, nalidixic acid and ciprofloxacin. It has pronounced inhibitory action against Candida glabrata, Candida albicans and Candida tropicalis isolated from women with vulvovaginal candidiasis, including three isolates resistant to azole drugs and amphotericin B. Basant displayed a high virucidal action against human immunodeficiency virus HIV-1NL4.3 in CEM-GFP reporter T and P4 (Hela-CD4-LTR-betaGal) cell lines with a 50% effective concentration (EC50) of 1:20000 dilution and nearly complete (98-99%) inhibition at 1:1000 dilution. It also prevented the entry of HIV-1(IIIB) virus into P4-CCR5 cells (EC50 approximately 1:2492). Two ingredients, Aloe and Amla, inhibited the transduction of human papillomavirus type 16 (HPV-16) pseudovirus in HeLa cells at concentrations far below those that are cytotoxic and those used in the formulation. Basant was found to be totally safe according to pre-clinical toxicology carried out on rabbit vagina after application for 7 consecutive days or twice daily for 3 weeks. Basant has the potential of regressing vulvovaginal candidiasis and preventing N. gonorrhoeae, HIV and HPV infections.
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PMID:A novel polyherbal microbicide with inhibitory effect on bacterial, fungal and viral genital pathogens. 1857 86

The presence, at the time of challenge, of antiviral effector T cells in the vaginal mucosa of female rhesus macaques immunized with live-attenuated simian-human immunodeficiency virus 89.6 (SHIV89.6) is associated with consistent and reproducible protection from pathogenic simian immunodeficiency virus (SIV) vaginal challenge (18). Here, we definitively demonstrate the protective role of the SIV-specific CD8(+) T-cell response in SHIV-immunized monkeys by CD8(+) lymphocyte depletion, an intervention that abrogated SHIV-mediated control of challenge virus replication and largely eliminated the SIV-specific T-cell responses in blood, lymph nodes, and genital mucosa. While in the T-cell-intact SHIV-immunized animals, polyfunctional and degranulating SIV-specific CD8(+) T cells were present in the genital tract and lymphoid tissues from the day of challenge until day 14 postchallenge, strikingly, expansion of SIV-specific CD8(+) T cells in the immunized monkeys was minimal and limited to the vagina. Thus, protection from uncontrolled SIV replication in animals immunized with attenuated SHIV89.6 is primarily mediated by CD8(+) T cells that do not undergo dramatic systemic expansion after SIV challenge. These findings demonstrate that despite, and perhaps because of, minimal systemic expansion of T cells at the time of challenge, a stable population of effector-cytotoxic CD8(+) T cells can provide significant protection from vaginal SIV challenge.
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PMID:With minimal systemic T-cell expansion, CD8+ T Cells mediate protection of rhesus macaques immunized with attenuated simian-human immunodeficiency virus SHIV89.6 from vaginal challenge with simian immunodeficiency virus. 1878 3

Live attenuated lentivirus immunization is the only vaccine strategy that elicits consistent protection against intravaginal challenge with pathogenic simian immunodeficiency virus (SIV). To determine the mechanism of protection in rhesus monkeys infected with attenuated simian-human immunodeficiency virus (SHIV)89.6, a detailed analysis of SIV Gag-specific T-cell responses in several tissues including the genital tract was performed. Six months after SHIV infection, antiviral T-cell responses were rare in the cervix; however, polyfunctional, cytokine-secreting, and degranulating SIV Gag-specific CD4(+) T cells were consistently found in the vagina of the immunized macaques. SIV-specific CD8(+) T cells were also detected in the vagina, blood, and genital lymph nodes of most of the animals. Thus, an attenuated SHIV vaccine induces persistent antiviral T cells in tissues, including the vagina, where these effector T-cell responses may mediate the consistent protection from vaginal SIV challenge observed in this model.
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PMID:Protective attenuated lentivirus immunization induces SIV-specific T cells in the genital tract of rhesus monkeys. 1907 81

The recently failed clinical efficacy trial of an acquired immunodeficiency syndrome (AIDS) vaccine that elicits antiviral CD8(+) T-cell responses has emphasized the challenge of producing an effective vaccine against human immunodeficiency virus (HIV). In the simian immunodeficiency virus (SIV)/ rhesus monkey model of AIDS, live-attenuated lentivirus 'vaccines' provide the best protection from uncontrolled viral replication and clinical disease after pathogenic SIV challenge. This review summarizes a recent series of studies in which we show that after vaginal SIV challenge of rhesus macaques immunized with an attenuated lentivirus protection from uncontrolled viral replication is primarily mediated by CD8(+) T cells in the vaginal mucosa. Immunization with a chimeric simian/human immunodeficiency virus (SHIV) results in a systemic infection that induces a moderate population of SIV-specific CD8(+) and CD4(+) T cells with cytolytic potential in the vaginal mucosa. Depletion of CD8(+) T cells at the time of SIV challenge completely abrogates the protection mediated by prior infection with attenuated SHIV. Further after vaginal SIV challenge, the only significant expansion of SIV-specific T cells occurs in the vagina in these animals. No significant expansion of T-cell responses was observed in systemic lymphoid tissues. Thus, the presence of SIV-specific CD8(+) T cells in the vagina on the day of vaginal SIV challenge and a modest expansion of local effector T cells is sufficient to stop uncontrolled SIV replication. It seems that T-cell based vaccine strategies that can elicit mucosal effector CD8(+) T-cell populations and avoid inducing systemic T-cell proliferation upon exposure to HIV have the greatest potential for mimicking the success of live-attenuated lentiviral vaccines.
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PMID:Antiviral CD8+ T cells in the genital tract control viral replication and delay progression to AIDS after vaginal SIV challenge in rhesus macaques immunized with virulence attenuated SHIV 89.6. 1909 61

Human immunodeficiency virus (HIV) has been shown to undergo self-destruction upon treatment of cell-free virions with partially double-stranded oligodeoxynucleotides targeting the polypurine tract (PPT) of the viral RNA in the virus particle. The ODN forms a local hybrid with the PPT activating the viral RNase H to prematurely cleave the genomic RNA. Here we are describing the self-destruction of a recombinant lentivirus harboring the PPT of HIV in a mouse vagina model. We showed a decrease in viral RNA levels in cell-free virus particles and a reduction reverse transcribed complementary DNA (cDNA) in virus-infected human and primary murine cells by incubation with ODNs. In the vagina simultaneous, prophylactic or therapeutic ODN treatments led to a significant reduction in viral RNA levels. Our finding may have some relevance for the design of other viral self-destruction approaches. It may lead to a microbicide for reduction of sexual and mother-to-child transmission.
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PMID:Retroviral self-inactivation in the mouse vagina induced by short DNA. 1918 51

Although there has been great progress in treating human immunodeficiency virus 1 (HIV-1) infection, preventing transmission has thus far proven an elusive goal. Indeed, recent trials of a candidate vaccine and microbicide have been disappointing, both for want of efficacy and concerns about increased rates of transmission. Nonetheless, studies of vaginal transmission in the simian immunodeficiency virus (SIV)-rhesus macaque (Macacca mulatta) model point to opportunities at the earliest stages of infection in which a vaccine or microbicide might be protective, by limiting the expansion of infected founder populations at the portal of entry. Here we show in this SIV-macaque model, that an outside-in endocervical mucosal signalling system, involving MIP-3alpha (also known as CCL20), plasmacytoid dendritic cells and CCR5(+ )cell-attracting chemokines produced by these cells, in combination with the innate immune and inflammatory responses to infection in both cervix and vagina, recruits CD4(+) T cells to fuel this obligate expansion. We then show that glycerol monolaurate-a widely used antimicrobial compound with inhibitory activity against the production of MIP-3alpha and other proinflammatory cytokines-can inhibit mucosal signalling and the innate and inflammatory response to HIV-1 and SIV in vitro, and in vivo it can protect rhesus macaques from acute infection despite repeated intra-vaginal exposure to high doses of SIV. This new approach, plausibly linked to interfering with innate host responses that recruit the target cells necessary to establish systemic infection, opens a promising new avenue for the development of effective interventions to block HIV-1 mucosal transmission.
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PMID:Glycerol monolaurate prevents mucosal SIV transmission. 1926 9

To reliably infect a primate model for human immunodeficiency virus (HIV), approximately 10,000-fold more virus must be delivered vaginally than intravenously. However, the vaginal mechanisms that help protect against HIV are poorly understood. Here, we report that human cervicovaginal mucus (CVM), obtained from donors with normal lactobacillus-dominated vaginal flora, efficiently traps HIV, causing it to diffuse more than 1,000-fold more slowly than it does in water. Lactobacilli acidify CVM to pH approximately 4 by continuously producing lactic acid. At this acidic pH, we found that lactic acid, but not HCl, abolished the negative surface charge on HIV without lysing the virus membrane. In contrast, in CVM neutralized to pH 6 to 7, as occurs when semen temporarily neutralizes the vagina, HIV maintained its native surface charge and diffused only 15-fold more slowly than it would in water. Thus, methods that can maintain both a high lactic acid content and acidity for CVM during coitus may contribute to both vaginal and penile protection by trapping HIV before it can reach target cells. Our results reveal that CVM likely plays an important but currently unappreciated role in decreasing the rate of HIV sexual transmission.
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PMID:Human immunodeficiency virus type 1 is trapped by acidic but not by neutralized human cervicovaginal mucus. 1969 70

The most common cause of mortality related to human papillomavirus (HPV) infection is cervical cancer. However, male HPV infection is also an important concern, both for the disease burden in men and for the risk of transmission to women. HPV is associated with a variety of cancers in men, including anal cancer and a subset of penile and oral cancers. The incidence of anal and oral cancers related to HPV is increasing in the general population and is growing even faster among individuals who are immunocompromised because of human immunodeficiency virus (HIV) infection. Penile HPV infection is very common among heterosexual men and remains high throughout a wide range of ages. Likewise, anal HPV infection and anal intraepithelial neoplasia are very common throughout a wide range of ages in both HIV-negative and HIV-positive men who have sex with men. Other HPV-related diseases of clinical importance in men include condylomata acuminata (genital warts) and recurrent respiratory papillomatosis. The quadrivalent HPV vaccine has been shown to be highly efficacious in the prevention of genital warts in women and precancerous lesions of the cervix, vulva, and vagina. In addition, recent interim data have shown that the quadrivalent HPV vaccine is highly effective in reducing external genital lesions in young men. Although the protective efficacy of HPV vaccination in men has not yet been fully established-pending the outcome of public policy discussions and cost-efficacy studies-there may be a strong rationale for vaccinating boys, similar to girls, at an early age when they have had limited or no prior sexual activity.
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PMID:Human papillomavirus-related disease in men: not just a women's issue. 2030 39

Sexual transmission of human immunodeficiency virus type 1 (HIV-1) accounts for 60-90% of new infections, especially in developing countries. During male-to-female transmission, the virus is typically deposited in the vagina as cell-free and cell-associated virions carried by semen. But semen is more than just a carrier for HIV-1. Evidence from in vitro and in vivo studies supports both inhibitory and enhancing effects. Intrinsic antiviral activity mediated by cationic antimicrobial peptides, cytotoxicity, and blockage of HIV-dendritic cell interactions are seminal plasma properties that inhibit HIV-1 infection. On the contrary, neutralization of vaginal acidic pH, enhanced virus-target cell attachment by seminal amyloid fibrils, opsonization by complement fragments, and electrostatic interactions are factors that facilitate HIV-1 infection. The end result, i.e., inhibition or enhancement of HIV mucosal infection, in vivo, likely depends on the summation of all these biological effects. More research is needed, especially in animal models, to dissect the role of these factors and establish their relevance in HIV-1 transmission.
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PMID:Role of semen in HIV-1 transmission: inhibitor or facilitator? 2108 39

Group B Streptococcus (GBS) is a leading cause of infectious morbidity in newborns. We describe the prevalence of GBS colonization and the serotypes and antibiotic susceptibility profiles of isolates obtained from a cohort of human immunodeficiency virus (HIV)-infected pregnant women. This was a cross-sectional study at a centre for the prevention of mother-to-child transmission of HIV. Vaginal and rectal swabs were collected at 35-37 weeks of gestation from 158 eligible women. GBS isolates were serotyped and antimicrobial susceptibility tests performed. Patient sociodemographic characteristics, CD4 counts and viral loads were abstracted from records. The overall anogenital prevalence of GBS colonization was 49/158 (31.0%): 40/158 (25.3%) for vagina, 19/158 (12.0%) for rectum and 10/158 (6.3%) for both. Predominant serotypes were Ib (34.9%) and Ia (25.6%). All were penicillin-susceptible. Two were resistant to erythromycin (4.0%) and one to clindamycin (2.0%). The colonization rate by GBS was high in this cohort. Serotype Ib was the most frequently identified.
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PMID:Group B Streptococcus in a cohort of HIV-infected pregnant women: prevalence of colonization, identification and antimicrobial susceptibility profile. 2167 24


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