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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epstein-Barr virus is an important aetiological factor in certain HIV-related syndromes, with its opportunist expression related to the level of host immunodeficiency. In asymptomatic people co-infected with HIV, EBV activity is reflected by increased viral shedding and rises in anti-EBV titres; as immunodeficiency ensues EBV manifests as epithelial hyperproliferation in OHL, and later as B-cell lymphoma in AIDS. The suggested role of EBV as a co-factor in the progression of HIV infection and development of AIDS has not been established, although another herpesvirus, cytomegalovirus, might play such a role. Advances in our understanding of HIV regulation and its interaction with other latent (herpes) viruses should provide important molecular and pharmacological approaches to the clinical management of advanced HIV disease.
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PMID:Acquired immunodeficiency syndrome and Epstein-Barr virus. 196 85

Our studies on pathology of AIDS point to four major conclusions. 1) The brain is often directly affected by the HIV infection (with the characteristics of subacute microglial encephalitis with pathognomonic multinucleated giant cells) and then by opportunistic infections such as Cytomegalovirus, Herpes-virus, Papova-virus JC (with progressive multifocal leucoencephalopathy), Mycobacterium tuberculosis, Toxoplasma gondii, Cryptococcus neoformans, Candida albicans and Aspergillus fumigatus; opportunistic neoplasms (i.e. B cell lymphoma mostly pluricentric) could also developed. 2) The heart is frequently involved as well; perivascular sclerosis and myocytolysis are the hallmarks of a peculiar cardiomyopathy. 3) In the lung viral, bacterial, fungal an protozoan severe infections are frequently present: common are those caused by Cytomegalovirus and Pneumocystis carinii. Frequently thin fibrotic interalveolar septa are observed (with consequent alteration of hematosis). 4) Adrenal (most frequently) and pituitary may display necrotic-hemorragic areas (in adrenals chiefly due to Cytomegalovirus). These may be extensive enough to explain the occurrence of clinical syndromes of endocrine insufficiency.
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PMID:[AIDS pathology: various critical considerations (especially regarding the brain, the heart, the lungs, the hypophysis and the adrenal glands]. 209 37

In incidence and epidemiology of sexually transmitted disease (STD)s in Southeast Asia and the Western Pacific, with gonorrhea, chancroid, nongonococcal urethritis, syphilis, genital herpes and genital warts at the forefront, are reviewed. The bacterial STDs gonorrhea, chancroid and syphilis are the major problems. Gonorrhea is the most prevalent STD in the region, with a high incidence of chromosomally-mediated resistant and penicillinase-producing strains comprising 35-53% of isolates. Clinical treatment failures due to spectinomycin-resistant gonococci are reported as increasing. Uncontrolled antibiotic sales are blamed for these resistant strains. Syphilis has declined in the 1950s, but has re-emerged. Chancroid is declining, while herpes is making up a greater share of ulcer disease. nongonococcal genital infection and chlamydia are thought to be the 2nd most common infection, however most centers do not have the facilities to isolate chlamydia. Genital warts are becoming a common cause for attendance at STD clinics and are a concern for cervical cancer. Prostitutes are most often cited as the source of male STD infection. The anonymity and large number of contacts of the sex industry, and high mobility of the indigenous population and of tourists are considered central in STD transmission. The high incidence of STDs in this area is a harbinger of future trends of HIV/AIDS in Asia.
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PMID:The epidemiology of sexually transmitted diseases in Southeast Asia and the western Pacific. 211 64

The main receptor for the human immunodeficiency viruses type 1 and 2 (HIV-1 and HIV-2) on T and B lymphocytes, monocytes and macrophages is the CD4 antigen 1-3. Infection of these cells is blocked by monoclonal antibodies to CD4(1,2) and by recombinant soluble CD4(4-9). Expression of transfected CD4 on the surface of HeLa and other human cells renders them susceptible to HIV infection 10. HIV-antibody complexes can also infect monocytes and macrophages by means of receptors for the Fc portion of immunoglobulins (FcR)11-13), or complement receptors 14,15. The expression of IgG FcRs can be induced in cells infected with human herpes viruses such as herpes simplex virus type 1 (HSV-1)16,17 and human cytomegalovirus (CMV)18-21. Here we demonstrate that FcRs induced by CMV allow immune complexes of HIV to infect fibroblasts otherwise not permissive to HIV infection. Infection was inhibited by prior incubation with human IgG, but not by anti-CD4 antibody or by recombinant soluble CD4. Once HIV had entered CMV-infected cells by means of the FcR, its replication could be enhanced by CMV transactivating factors. Synergism between HIV and herpes viruses could also operate in vivo, enhancing immunosuppression and permitting the spread of HIV to cells not expressing CD4.
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PMID:HIV susceptibility conferred to human fibroblasts by cytomegalovirus-induced Fc receptor. 215 97

We determined IgG antibodies against Human Herpesvirus-6 (strain Uganda 1102, M. D. Griffin, London) in the indirect immunofluorescence test in sera from 1105 persons of various age groups. Of these sera 570 were retested using HHV-6 strain St. W. (Prof. Schneweis, Bonn). We could confirm that maternal antibodies decrease between birth and six months of age and the seropositive rate rises rapidly between seven months and five years of age up to 79.5%. Between six and ten years and up to 40 years, the antibody-positive rate lies around 81.3% and 66%, respectively. To confirm the causal nature of human herpes virus type 6 (HHV-6) for exanthema subitum we could demonstrate eight seroconversions testing sera from 14 patients with roseola infantum. In addition, the virus was isolated from peripheral blood lymphocytes of children during the acute fever phase in four cases in tissue culture and in six cases the virus was detected by positive hybridization. In single and some paired sera from patients with acute exanthematous diseases, rubella (n = 28), parvovirus B 19 (n = 24), measles (n = 17), mumps (n = 27), adenovirus (n = 27) and parinfluenza virus type 3 (n = 28) and in sera from patients with Kawasaki syndrome (n = 20), acute varicella-zoster- (n = 27), acute herpes simplex- (n = 18) and HIV-1 infection (n = 50), we found no HHV-6 IgM antibodies and no HHV-6 IgG antibody rises. We could only demonstrate an HHV-6 seropositive rate according to our age-prevalence study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of antibodies to human herpesvirus 6 in different age groups, in children with exanthema subitum, other acute exanthematous childhood diseases, Kawasaki syndrome, and acute infections with other herpesviruses and HIV. 215 75

Kaposi's sarcoma (KS) (Kaposi, 1872) is classified into at least three forms: 1) the classic form; in elderly men of southern European, Jewish, and Italian origin, 2) the endemic form; among native populations in equatorial Africa and 3) the epidemic form; as a complication of AIDS. As one additional form could be posttransplantation KS in organ transplant recipients. Histologically, KS is composed of two characteristic features; a proliferation of angiomatous lesion and of spindle-shaped cells. The pathological entity of the disease is still controversial. As a cause of the disease, human cytomegalovirus (HCMV) has been the subject based on epidemiologic, serologic, geopathologic and histopathologic observations. About half of KS cases with AIDS has shown evidence of HCMV infection as cytomegalic viral inclusions of the cells. In contrast, about 30% of AIDS cases without KS showed histological HCMV infection. A connection between HCMV and KS was suggested by the detection of herpes-type virus particles in several KS tissue culture lines and in a tumor specimen. DNA and RNA homologous with HCMV sequences have been detected in tumor tissue of both endemic and epidemic KS by electrophoretic methods. HCMV sequences was detected in extracted DNA of 30% of classic KS, using Southern blot technique. In situ hybridization technique using specific DNA probes for HCMV has been developed to reveal endogenous nucleic acid sequences in fixed tissue sections. However, some reports showed that by the in situ technique only a small number of KS cells in the AIDS cases and no case of the classic KS were positive for HCMV within KS lesions. HCMV infections are ubiquitous. There is a very high seropositivity of HCMV in African inhabitants as well as in Africans with endemic KS. A strong association between HCMV and KS was not known. As for HIV itself in AIDS with KS, previous studies have showed the presence of chromosomal abnormalities of KS cells, but not revealed the presence of HIV DNA sequences in KS. Vascular tumors were produced by NIH/3T3 cells transfected with KS DNA of AIDS. An oncogene isolated by transfection of KS DNA encodes a growth factor; FGF. Isolation of rearranged human transforming gene following transfection of KS DNA was performed. DNA having transforming genetic elements which have been repetitively transmitted into phenotypically normal NIH/3T3 cells through cycles of transfection was isolated from tissues of KS with AIDS.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Kaposi's sarcoma]. 215 69

Three patients with predominantly sensory neuropathy in course of HIV-1 infection are reported. In all cases ultrastructural examination showed herpes virus-like particles in the axoplasmic matrix of myelinated fibers and in endoneurial macrophages. In 2 cases clinical patterns of posterior column involvement were observed.
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PMID:AIDS--associated predominantly sensory neuropathy. The role of herpes viruses. 215 87

24 natural membrane condoms of 2 brand were tested in a static bath for leakage of a small virus, PhiX174, 27 nm in diameter, and a larger virus, Herpes Simplex Virus Type I, 120-150 nm in diameter, in a 4-hour experiment. These viruses were chosen because the bacteriophage PhiX174 is slightly smaller than Hepatitis B and is easy and safe to assay, and Herpes virus is close in size and chemical composition to HIV, and is relatively easy to assay on mouse kidney cells. For the test 40 million plaque forming units (pfu/ml of PhiX174 and 1 million herpes simplex pfu/ml were incubated in a condom suspended in a beaker containing Dulbecco's phosphate buffer, with magnetic stirring. 10 to 24 condoms of Brand A and 13 of 24 Brand B leaked some phage. 2 condoms leaked some herpes virus. The results were computed into an index of barrier function, the barrier ratio. There was a variation in leakage over 2 orders of magnitude between condoms. The results in this status situation were similar to those obtained by others in a simulated active coitus experiment, in that greater amounts of the smaller viruses leaked through natural condoms.
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PMID:Virus leakage through natural membrane condoms. 216 14

Because of the various neoplastic manifestations of human immunodeficiency virus (HIV) and the variable period between HIV infection and the development of tumors related to acquired immunodeficiency syndrome (AIDS), it is possible that certain behaviors, toxins, genes, or infectious agents--particularly viruses--may act as cofactors in the pathogenesis of AIDS-related neoplasms. Most epidemiologic and laboratory investigations of possible cofactors have been directed toward Kaposi's sarcoma (KS), by far the most common AIDS-related tumor and one closely associated with male homosexual lifestyle in the U.S. Nonetheless, epidemiologic investigations of putative associations have not demonstrated any clear association between KS and particular viruses. Furthermore, laboratory investigations, both serologic and molecular/genetic, have failed to definitively implicate as cofactors for KS these viruses: cytomegalovirus, Epstein-Barr virus (EBV), herpes simplex viruses, pathogenic human papillomaviruses, or human herpes virus type 6. Investigations of a suggested association between EBV and AIDS-associated non-Hodgkin's (B cell) lymphomas (NHLs) have also been inconclusive. However, HIV may act as a cofactor in accelerating the development of hepatitis B-associated hepatocellular carcinoma. In summary, viral or other cofactors have not been definitely identified as cofactors in AIDS-related tumors.
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PMID:Possible cofactors for the development of AIDS-related neoplasms. 216 69

Herpetic ocular disease is one of the major causes of corneal blindness. Clinical diagnosis of corneal disease is based principally on corneal appearance. However, abnormal morphology of the corneal epithelium (CE) is not an indicator for the presence of a herpes virus. Further, it has not been established if herpes viruses are present in normal corneal epithelial tissue. In these studies, the polymerase chain reaction was used to evaluate normal and diseased corneal epithelium for the presence of herpes simplex virus type 1 (HSV-1), Epstein-Barr virus (EBV) and cytomegalovirus (CMV) genomic sequences. Thirty-two normal corneal epithelium specimens obtained from cadavers shortly after death were analyzed for HSV-1, EBV and CMV genomic sequences. Three of the 32 normal CE specimens were positive for amplified EBV DNA, 1 was positive for HSV-1 DNA, and none was positive for CMV DNA. We also tested eight herpetic dendritic lesions of which 3 were HSV-1 culture and PCR positive. The remaining five dendritic lesions were HSV-1 culture and PCR negative. Since these lesions were not evaluated for other herpesviruses, the etiology of these dendritic lesions is unknown. Six corneal epithelium samples from HIV-infected donors were negative for EBV, CMV and HSV-1 amplified sequences. Positive EBV, CMV and HSV-1 serology on all normal donors and on donors with clinically apparent disease did not correlate with positive PCR results. The results of these studies suggest that EBV and HSV-1 DNA can be amplified from a small percentage of apparently normal corneal epithelium.
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PMID:Detection of herpes viral genomes in normal and diseased corneal epithelium. 216 92


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