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)

Monocytes treated with interferon-alpha (IFN-alpha) at virus challenge show no evidence of human immunodeficiency virus (HIV) infection: no p24 antigen or reverse transcriptase (RT) activity, no viral mRNA and no proviral DNA. Levels of p24 antigen and RT activity in monocytes infected with HIV 1-3 weeks before IFN-alpha treatment gradually decrease to baseline. HIV-induced cytopathic changes are markedly reduced, as are levels of HIV mRNA: the frequency of productively infected cells is less than or equal to 1%. But, levels of proviral DNA in the IFN-alpha-treated and control HIV-infected cells are indistinguishable, and remain so through 3 weeks. Large quantities of proviral DNA in IFN-alpha-treated cells with little active transcription suggest true microbiological latency. The major potential source for IFN-alpha in HIV-infected patients is the macrophage. With any of 15 virus isolates, tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, IFN-omega or IFN-beta are not detected nor the mRNA expressed in HIV-infected or uninfected monocytes. Both uninfected and HIV-infected monocytes produce high levels of these cytokines after treatment with synthetic double-stranded RNA (poly-I:C). Uninfected monocytes also produce high levels of IFN-alpha after treatment with Poly-I:C, Newcastle disease virus or herpes simplex virus. In marked contrast, HIV-infected monocytes express no IFN-alpha activity or mRNA before or after treatment with any of these agents. The markedly diminished capacity of HIV-infected monocyte to produce IFN-alpha reflects a specific transcriptional block and may be an adaptive mechanism of virus to alter basic microbicidal functions of this cell.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of cytokine and viral gene expression in monocytes infected with the human immunodeficiency virus. 188 15

Toward gene therapy for the treatment of human immunodeficiency virus type 1 (HIV-1) infections in AIDS, Moloney murine leukemia virus-derived retroviral vectors were engineered to allow constitutive and tat-inducible expression of an HIV-1 5' leader sequence-specific ribozyme (Rz1). These vectors were used to infect the human CD4+ lymphocyte-derived MT4 cell line. The stable MT4 transformants expressing an HIV-1 RNA-specific ribozyme, under the control of the herpes simplex virus thymidine kinase (tk) promoter, were found to be somewhat resistant to HIV-1 infection as virus production was delayed. In cells allowing ribozyme expression under control of the simian virus 40 or cytomegalovirus promoter, the rate of HIV-1 multiplication was slightly decreased, and virus production was delayed by about 14 days. The highest level of resistance to HIV-1 infection was observed in MT4 cells transformed with a vector containing a fusion tk-TAR (trans activation-responsive) promoter to allow ribozyme expression in a constitutive and tat-inducible manner; no HIV-1 production was observed 22 days after infection of these cells. These results indicate that retroviral vectors expressing HIV-1 RNA-specific ribozymes can be used to confer resistance to HIV-1 infection.
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PMID:Resistance to human immunodeficiency virus type 1 (HIV-1) infection in human CD4+ lymphocyte-derived cell lines conferred by using retroviral vectors expressing an HIV-1 RNA-specific ribozyme. 189 2

As the human immunodeficiency virus is being detected in increasing numbers of asymptomatic individuals at risk, newer earlier patterns of disease have become apparent--including cranial and cervical herpes zoster, oral hairy leukoplakia, and oral candidiasis--thus linking viral and other disease to the development of acquired immunodeficiency disease (AIDS). Many similarities between patients with AIDS and other immunosuppressed patients have emerged. As immunosuppressed patients survive longer, they begin to manifest cancers such as lymphomas and squamous cell cancers in addition to Kaposi's sarcoma. Otolaryngologists can learn to identify and treat otitis and sinusitis in the immunosuppressed patient, to identify predictive early signs such as oral hairy leukoplakia, herpes simplex virus, and oral candidiasis, and to diagnose and treat Kaposi's sarcomas of the head and neck, lymphomas, squamous cell cancers, and opportunistic infections as the immunodeficiency disease progresses.
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PMID:Otolaryngology problems in the immune compromised patient--an evolving natural history. 190 Nov 47

The sexually transmissible pathogenic microorganisms, which are also capable of initiating pre- or perinatal infections, include Neisseria gonorrhoeae, Treponema pallidum, Chlamydia trachomatis serovars D through K, group B streptococci, urogenital mycoplasmas, herpes simplex viruses types I and II, cytomegalovirus, hepatitis B virus, human immunodeficiency viruses, human papillomaviruses, Candida spp. and Trichomonas vaginalis. With special emphasis on paediatric and neonatological aspects, brief discussions of the following topics are presented: the epidemiology of these agents, the diseases they can induce in pregnancy, the mode of infection of and the diseases in the fetus and neonate, the preventive measures, the diagnosis and therapy.
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PMID:[Pre- and perinatal infections with sexually transmissible microorganisms]. 192 15

Earlier diagnosis and improved therapies for the opportunistic infections have led to improved quality of life as well as survival time of patients with advanced HIV-related immunodeficiency. Most of the therapies can be administered on an outpatient basis. Outpatient treatment further contributes to improving the quality of life of the patients. Presentation, clinical aspects, treatment and prophylaxis of the five most frequent opportunistic infections in HIV-infected patients with advanced immunodeficiency in our outpatient clinic (oral and esophageal candidiasis, pneumocystis carinii pneumonia, herpes zoster, herpes simplex virus infection and cerebral toxoplasmosis) are discussed with respect to the practical implications.
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PMID:[Ambulatory therapy and prevention of the most frequent HIV-associated opportunistic infections]. 192 48

Herpes simplex infection of the genitals is a common condition, more often due to herpes simplex virus (HSV) type 2 than to type 1 virus. There is a severe first attack followed by mild recurrences which are more common and more frequent after HSV-2 than after HSV-1 genital infection. Clinical features with prodrome, vesicles and erosions may be characteristic allowing rapid clinical diagnosis. When possible laboratory confirmation should be attempted. General management includes simple hygiene, avoidance of sexual transmission, use of condoms, and notifying partners. Oral acyclovir (Zovirax, Wellcome) is the drug of choice for initial attacks and should be considered for all women with this diagnosis. Intravenous acyclovir may be used for very severe attacks. Men with initial attacks may be treated with oral acyclovir but mild disease affecting only skin may be treated with 5% acyclovir cream. Recurrences are short so acyclovir has less effect. Frequent recurrences can be troublesome and may be suppressed by continuous oral acyclovir, or individual attacks may be aborted with intermittent therapy. Various systemic complications may occur; an important but rare problem is primary herpes in late pregnancy. Acyclovir is effective in the treatment of the troublesome herpes simplex disease associated with human immunodeficiency infection. Acyclovir is one of the more expensive treatments for sexually transmitted diseases. At present in many countries costs are being examined, and application of the principles outlined here should help to minimize cost and maximize care.
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PMID:Management of genital herpes simplex infection. 195 14

Infectious herpes simplex virus type 1 (HSV-1) recombinants were constructed by inserting the cDNA sequence of the human immunodeficiency virus type 1 (HIV-1) gag gene (from nucleotide position 675 [SacI] to 3859 [Asp718] of the cDNA sequences of HIV-1 strain BH-10) within the DNA sequences of the BamHI DNA fragment B of the genome of an apathogenic HSV-1 strain HFEM. This HSV-1 strain possesses a 4.1-kbp deletion within the BamHI DNA fragment B between 0.762 and 0.789 map units of the viral genome, which allows the insertion of at least 4 kbp of foreign genetic material into this particular region. The DNA sequences of the immediate early promoter (IE4) of HSV-1 that were inserted upstream from the gag gene were used as a promoter. The screening of 205 virus stocks derived from individual plaques revealed that 46 recombinant viruses harbor HIV-1 gag-specific DNA sequences. However, it was found that only six of the recombinant viruses are able to express the gag gene product of HIV-1. This indicates that the ratio of the positive recombination events is about 2.9%.
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PMID:Expression of human immunodeficiency virus type 1 gag gene using genetically engineered herpes simplex virus type 1 recombinants. 196 77

9-Cyclobutyladenine (4a), cis- and trans-9-[3- (hydroxymethyl)cyclobutyl]adenine (4b) and 9-[3,3-bis(hydroxymethyl)cyclobutyl]adenine(4d) were prepared from the corresponding cyclobutylamine derivatives (1a, 1b and 1d). Guanine congeners (9a, cis- and trans-9b and 9d) and carbocyclic oxetanocin G (1',2'-trans-9f) were also prepared. Carbocyclic oxetanocin A(1',2'-trans-4f), the preparation of which we have already published, and G were found to be active against herpes simplex virus (type 1 and 2) in vitro, while cis-4b and cis-9b showed an in vitro antiretroviral activity against human immunodeficiency virus (type 1).
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PMID:Synthesis and antiviral activities of carbocyclic oxetanocin analogues. 196 11

The prevalence of viral and bacterial sexually transmitted diseases were studied in 101 men attending a dermatovenereal outpatient clinic in Mogadishu. A control group of 103 healthy adult men were included for the serological part of the study. Serological markers of hepatitis B virus (HBV), human immunodeficiency virus (HIV), cytomegalovirus (CMV) and herpes simplex virus (HSV) were studied. All sera were tested for syphilis markers. HBV serum markers were detected in 84% of the men in the study group and 66% of the healthy controls (P less than 0.005). Hepatitis B virus carriers were detected more frequently in the study group than among the controls. Also, 96% of the men in both groups had CMV antibodies and all of them had antibodies to HSV. No sera were found to contain HIV antibodies. The TPHA-positivity was 10% and 3% in the study and control groups respectively, and 5% of the patients had syphilis IgM antibodies. Sexual contact with prostitutes was recorded in 54% and 48% respectively of patients and controls, and such contact was correlated with TPHA-positivity in the study group. Chlamydia trachomatis antigen was detected in urogenital specimens of 14% of the men in the study group and gonococcal culture was positive in 53% of those with urethral discharge.
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PMID:Sexually transmitted diseases in men in Mogadishu, Somalia. 196 90

Functional impairment and selective depletion of CD4+ T cells, the hallmark of AIDS, are at least partly caused by human immunodeficiency virus (HIV-1) type 1 binding to the CD4 molecule and infecting CD4+ cells. It may, therefore, be of therapeutic value to target an antiviral agent to CD4+ cells to prevent infection and to inhibit HIV-1 production in patients' CD4+ cells which contain proviral DNA. We report here that HIV-1 replication in normal primary CD4+ T cells can be inhibited by pokeweed antiviral protein, a plant protein of relative molecular mass 30,000, which inhibits replication of certain plant RNA viruses, and of herpes simplex virus, poliovirus and influenza virus. Targeting pokeweed antiviral protein to CD4+ T cells by conjugating it to monoclonal antibodies reactive with CD5, CD7 or CD4 expressed on CD4+ cells, increased its anti-HIV potency up to 1,000-fold. HIV-1 replication is inhibited at picomolar concentrations of conjugates of pokeweed antiviral protein and monoclonal antibodies, which do not inhibit proliferation of normal CD4+ T cells or CD4-dependent responses. These conjugates inhibit HIV-1 protein synthesis and also strongly inhibit HIV-1 production in activated CD4+ T cells from infected patients.
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PMID:Inhibition of HIV replication by pokeweed antiviral protein targeted to CD4+ cells by monoclonal antibodies. 197 41


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