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At least 19 recordsLinked to original sources
PubMed1995

In vivo fate of HIV-1-infected T cells: quantitative analysis of the transition to stable latency.

Although it is presumed that the integration of HIV-1 into the genome of infected CD4+ T lymphocytes allows viral persistence, there has been little direct evidence that CD4+ T cells with integrated provirus function as a latent reservoir for HIV-1 in infected individuals. Using resting CD4+ T-cell populations of extremely high purity and a novel assay that selectively and unambiguously detects integrated HIV-1, we show that resting CD4+ T cells harbouring integrated provirus are present in some infected individuals. However, these cells do not accumulate within the circulating pool of resting CD4+ T cells in the early stages of HIV-1 infection and do not accumulate even after prolonged periods in long-term survivors of HIV-1 infection. These results suggest that because of viral cytopathic effects and/or host effector mechanisms, productively infected CD4+ T cells do not generally survive for long enough to revert to a resting memory state in vivo.

Base Sequence↗
PubMed1995

Virus burden in long-term survivors of human immunodeficiency virus (HIV) infection is a determinant of anti-HIV CD8+ lymphocyte activity.

Persons infected with human immunodeficiency virus (HIV) for > 8 years were studied to delineate virologic and immunologic attributes of long-term survival. Whereas those with 300-700 CD4+ cells/microL often had circulating cytotoxic T lymphocytes (CTL) against HIV antigens, those with > 1000 CD4+ cells/microL did not. The subjects with > 1000 CD4+ cells/microL had low virus burden, low levels of Gag-specific CTL precursors, and minimal CD8+ cell activation. Overall, elevated levels of CD8+ cells, CD38 antigen expression on CD8+ cells, and anti-HIV functions were correlated with increased virus burden, provirus load, and HIV plasma RNA levels. A factor that suppressed HIV replication was spontaneously secreted from CD8+ cells of most subjects but not from those with high CD4+ cell counts. CD8+ cell activities, therefore, may reflect chronic viral stimulation of the immune system. Long-term survivors with high levels of CD4+ cells maintained control of viral replication but lacked the CD8+ cell activities.

ADP-ribosyl Cyclase↗
PubMed1995

Biological characterization of nef in long-term survivors of human immunodeficiency virus type 1 infection.

We have previously shown that there were no gross deletions or obvious sequence abnormalities within nef of human immunodeficiency virus type 1 (HIV-1) in the 10 long-term survivors studied (Y. Huang, L. Zhang, and D. D. Ho, J. Virol. 69:93-100, 1995). Here we extend our study to examine these nef alleles in a functional context. Using a new technique, termed site-directed gene replacement, we have precisely replaced the nef of an infectious molecular clone, HIV-1HXB2, with nef alleles derived from 10 long-term survivors as well as from a patient with AIDS. The replication properties of these chimeric viruses demonstrated that the nef alleles derived from long-term survivors neither significantly increased nor decreased viral replication, compared with the nef allele of Nef+ HIV-1HXB2 and that derived from a patient with AIDS. However, Nef+ viruses always replicated faster than virus lacking nef. Moreover, single-cell infection analysis by the MAGI assay showed that these chimeric viruses, as well as Nef+ HIV-1HXB2, were more infectious than Nef- HIV-1HXB2 was. Therefore, we conclude that the genotypic and phenotypic features of nef are not likely to account for the nonprogression of HIV-1 infection in the 10 cases studied, unless the function of the nef gene in vivo is not accurately reflected by the in vitro assays we used.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Effects of TH1 and TH2 cytokines on CD8+ cell response against human immunodeficiency virus: implications for long-term survival.

CD8+ cells from long-term survivors [LTS; infected with human immunodeficiency virus (HIV) for 10 or more years and having CD4+ cell counts of > or = 500 cells per microliters] have a 3-fold greater ability to suppress HIV replication than do CD8+ cells from patients who have progressed to disease (progressors) during the same time period. A change in the pattern of cytokines produced in the host from those that typically favor cell-mediated immunity (T helper 1, TH1 or type 1) to those that down-regulate it (T helper 2, TH2 or type 2) was investigated as a cause of this reduced CD8+ cell anti-HIV function. Treatment of CD8+ cells from LTS with the TH1 cytokine interleukin (IL)-2 enhanced their anti-HIV activity, whereas exposure of these cells to TH2 cytokines IL-4 or IL-10 reduced their ability to suppress HIV replication and to produce IL-2. IL-2 could prevent and reverse the inhibitory effects of IL-4 and IL-10. Moreover, prolonged exposure of CD8+ cells from some progressors to IL-2 improved the ability of these cells to suppress HIV replication. These observations support previous findings suggesting that strong CD8+ cell responses play an important role in maintaining an asymptomatic state in HIV infection. The data suggest that the loss of CD8+ cell suppression of HIV replication associated with disease progression results from a shift in cytokine production within the infected host from a TH1 to a TH2 pattern. Modulation of these cytokines could provide benefit to HIV-infected individuals by improving their CD8+ cell anti-HIV activity.

CD4-Positive T-Lymphocytes↗
PubMed1991

Adult survivors of childhood sexual abuse and subsequent risk of HIV infection.

BACKGROUND: Epidemiologic description of long-term adverse health effects of childhood sexual abuse is lacking, despite estimates that perhaps 30 percent of adults have experienced sexual assault in childhood. METHODS: In an adult cohort enrolled to investigate causes of transmission of human immunodeficiency virus, we identified current behaviors affecting risk of infection that were associated with a history of early sexual abuse. One hundred and eighty-six individuals provided information on the occurrence of abuse and subsequent sexual and drug using activities. RESULTS: Approximately half of the women and one-fifth of the men reported a history of rape during childhood or adulthood. Twenty-eight percent of the women and 15 percent of the men recalled that they had been sexually assaulted during childhood. People who reported childhood rape compared with people who did not were four times more likely to be working as prostitutes (90 percent confidence interval = 2.0, 8.0). Women were nearly three times more likely to become pregnant before the age of 18 (90% CI = 1.6, 4.1). Men who reported a history of sexual abuse had a twofold increase in prevalence of HIV infection relative to unabused men (90% CI = 1.0, 3.9). CONCLUSIONS: The disturbing prevalence of early sexual abuse and its possible health-related consequences call for prompt and routine investigation of sexual abuse histories. Identification of sexual victimization may be an important component for management of risk factors for human immunodeficiency virus.

Adolescent↗
PubMedDate not supplied

HIV infection and rheumatic diseases--autoimmune mechanisms in immunodeficient hosts.

The recognition of a newly acquired immunodeficiency syndrome (AIDS) in 1981 has had dramatic social and economic implications. Eventually, an epidemic of the viral infection developed with a potential to spread globally. The extraordinary breadth of AIDS research lead to the early identification of the causative agent: The human immunodeficiency virus (HIV) is a member of the lentivirus family and is characterized by its ability to remain latent within the genome of the infected host. The primary targets for the HIV are helper T-lymphocytes and monocytes/macrophages, which results in the progressive destruction of immune functions in the infected hosts. Binding to and entry into the cells is facilitated by a high-affinity interaction of a viral glycoprotein and the CD4 molecule. Signs of the immunodeficient state, manifested as a broad spectrum of opportunistic infections initially dominated the clinical presentations of HIV infected patients. Over the last decade, however, the manifestations of HIV infection have steadily grown and, surprisingly, include many rheumatic syndromes and autoimmune phenomena. The finding that HIV-infected individuals present with a highly progressive form of Reiter's syndrome and psoriasis has challenged our understanding of immune functions in HLA-B27 associated disorders. Obviously, CD8+ T-cells can maintain function despite the depletion of CD4+ helper T-cells. Consistent with the current model of the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus, patients with these syndromes were described to go into remission when CD4+ T-cells were selectively depleted in active HIV infection. There is growing evidence that complex mechanisms arise from the interaction of the HIV and the human host which extend beyond the initial expectation that the virus only kills CD4+ helper T-cells. Indicating yet another aspect of HIV disease, a new syndrome mimicking Sjögren's syndrome has been encountered in HIV-infected patients and has been named the diffuse infiltrative lymphocytosis syndrome. Dense infiltrates of CD8+, potentially antiviral killer cells, are characteristically found in the salivary glands of patients who express a certain HLA genotype and who are, typically, long-term survivors of the disease. Recent reports have stressed a new mechanism of disease induction in HIV infected patients. Inappropriate induction of potentially destructive cytokines appears to be initiated by the viral infection and the expression of the viral genome seems to be effectively modulated by cytokines. In summary, HIV infection may provide important insights in the pathogenesis of rheumatic diseases co-occurring with HIV infections.(ABSTRACT TRUNCATED AT 400 WORDS)

Arthritis, Rheumatoid↗
PubMed1990

Inhibitory effects of 9-(2-phosphonylmethoxyethyl)adenine and 3'-azido-2',3'-dideoxythymidine on tumor development in mice inoculated intracerebrally with Moloney murine sarcoma virus.

9-(2-Phosphonylmethoxyethyl)adenine (PMEA), a potent inhibitor of human immunodeficiency virus (HIV), caused a dose-dependent suppression of tumor formation, and mortality associated therewith, in 6-day-old NMRI mice inoculated intracerebrally with Moloney murine sarcoma virus (MSV). Even at a dose as low as 1 mg/kg/day, PMEA effected a significant delay in tumor formation. When evaluated in parallel with PMEA, 3'-azido-2',3'-dideoxythymidine (AZT) conferred a comparable tumor-inhibitory effect at a 5- to 10-fold higher dose than PMEA. Prolonged treatment of MSV-infected mice with PMEA resulted in long-term survivors without apparent signs of tumor development. In view of the propensity of HIV to spread to the central nervous system (CNS), the marked activity shown by PMEA against experimental retrovirus infection of the brain in mice points to its potential in the treatment of AIDS and other retrovirus infections of the CNS.

Adenine↗
PubMed1988

Anorectal and colonic disease and the immunocompromised host.

The immunocompromised host is becoming increasingly ubiquitous in the authors' patient population. There are growing numbers of long-term transplant recipients, and combination chemotherapy is producing many long-term survivors. Of greatest concern is that the number of patients with human immunodeficiency virus (HIV) causing immunosuppression is increasing. The literature is reviewed to produce a current summary of conditions affecting the anorectum and colon and arising as a direct consequence of the immunocompromised host. Pathophysiology and theoretic considerations are mentioned where applicable and current therapy is discussed. The conditions are classified under infectious, neoplastic, iatrogenic, and congenital. Although the colorectal surgeon will encounter most of these conditions sometime during a career, many are infrequent, and a current review is provided herein to provide categorization and updated information.

Colonic Diseases↗
PubMed1995

Persistence of attenuated rev genes in a human immunodeficiency virus type 1-infected asymptomatic individual.

With the goal of examining the functional diversity of human immunodeficiency virus type 1 (HIV-1) env genes within the peripheral blood mononuclear cells of an asymptomatic individual, we substituted four complete env genes into the replication-competent NL4-3 provirus. Despite encoding full-length open reading frames for gp120 and gp41 and the second coding exon of tat and rev, each chimera was replication defective. Site-directed mutagenesis of codon 78 in the Rev activation domain (from a hitherto unique Ile to the subtype B consensus Leu) partially restored infectivity for two of three chimeras tested. Similarly, mutagenesis of rev codon 78 of NL4-3 from Leu to Ile partially attenuated this virus. Ile-78 was found in all 13 clones examined from samples taken from this asymptomatic subject 4.5 years after infection, including 9 from peripheral blood mononuclear cells and 4 from a virus isolate, as well as 4 additional clones each from peripheral blood mononuclear cells sampled 37 and 51 months later. We next examined conservation of the Rev activation domain within and among long-term survivors (LTS) and patients with AIDS, as well as T-cell-line-adapted strains of HIV-1. Putative attenuating mutations were found in a minority of sequences from all five LTS and two of four patients with AIDS. Of the 11 T-cell-line-adapted viruses examined, none had these changes. Among and within LTS virus population had marginally higher levels of diversity in Rev than in Env; patients with AIDS had similar levels of diversity in the two reading frames; and T-cell-line-adapted viruses had higher levels of diversity in Env. These results are consistent with the hypothesis that asymptomatic individuals harbor attenuated variants of HIV-1 which correlate with and contribute to their lack of disease progression.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Reiter's syndrome and associated arthritides.

Several distinct arthritic syndromes now have been recognized in HIV-infected persons. These comprise seronegative spondarthritis, including classic Reiter's syndrome and psoriatic arthritis associated with HLA-B27, and undifferentiated arthritis usually confined to the lower limbs, unassociated with other lesions, and unrelated to any known genetic marker. In such cases great care should be taken to exclude infection. In addition, a syndrome of short-lived but sometimes severe arthralgias also occurs. Spinal pain is a major problem in some patients but ankylosing spondylitis appears to be rare among this group. Psoriasis probably occurs more often in the HIV-infected group than in the population in general and may be especially severe in those patients with arthritis. Arthritis has been reported in the United States, Europe, and Africa among persons considered to be at high and low risk for HIV infection. Arthritis can occur at any stage of HIV infection, but the true prevalence of arthritic syndromes and the nature of their association with HIV infection remains unclear. In view of the development of Reiter's syndrome in some patients, precipitating bacterial infections have been sought as the culprits. In a minority of cases, shigella, yersinia, and campylobacter infections have been implicated, but in the majority of cases, no specific infection has been identified. In most patients depletion of circulating CD4-positive lymphocytes is present by the time that arthritis is detected, but only limited data on synovial immunopathology are available. In some patients changes of nonspecific chronic synovial inflammation are present and synovial fluid cell counts are high. In other patients evidence of inflammatory changes is minimal. Human immunodeficiency virus has been isolated from joint fluid and identified in large mononuclear, probably dendritic, cells and lymphocytes. Synovium from patients dying with AIDS but with apparently normal joints also shows significant abnormalities that could lead to joint disease in long-term survivors. The possibility of a viral etiology of arthritis in some cases is suggested by the induction of arthritis in animals by lentivirus infection; it also is possible, however, that HIV enhances the effect of mechanisms that can operate in the absence of HIV infection. Conventional treatments of rheumatic lesions, including intraarticular steroids, appear to be safe and reasonably effective. Anecdotal evidence suggests that treatment with methotrexate and azathioprine leads to exacerbation of HIV disease and should be avoided.

Arthritis↗
PubMed1991

[Surgical treatment of right-sided infective endocarditis].

Between 1980 and 1989, 8 patients (5 men, 3 women; mean age 30 years) were operated upon in our department of right-sided infective endocarditis. Six patients were heroin addicts and among these 3 were HIV positive and 2 had confirmed AIDS. The most frequently encountered microorganisms (6 cases) were staphylococci. It was decided to operate because of persistent infection and haemodynamic deterioration. The infection involved the pulmonary valve in only 1 of the 8 patients. Surgery was performed during the acute phase in 5 patients and was conservative in 6 patients, consisting of excision of the vegetations or valvulectomy combined or not with valvuloplasty. A high mortality rate (3/8 cases) was observed only among patients operated upon in the acute phase. This may be due to the underlying immunodeficiency and poor haemodynamic state of these patients. Among survivors, the long-term results were excellent, with no recurrent endocarditis and no death, and with only one subsequent operation, 4 years after the first one, for residual tricuspic valve regurgitation. This study shows that patients with right-sided infective endocarditis should be operated upon outside the acute phase of the disease and as soon as complications appear, and that surgery should preferably be conservative.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Evaluation of prognosis and survival of the HIV-infected patient.

HIV disease, once considered an acute disease with a 100% mortality rate but a very short symptomatic stage, has begun to emerge as a preventable, treatable, chronic disease. Interactions between patients, dentists, and physicians are essential to gain the information necessary to provide appropriate dental care for both short-term and long-term survivors. The prognosis and survival time of the dental patient may influence treatment protocols and necessitate modified dental procedures. Certain clinical and laboratory parameters, which may be useful indicators of disease progression, need to be recognized by the dental clinician. These parameters include systemic signs, symptoms, and serologic data as well as intraoral manifestations associated with HIV disease. Although a perfect classification system for progression of HIV disease does not exist, trends among larger cohorts may enable health care providers to estimate the prognosis and survival of HIV-infected patients on an individual basis. This article presents clinical and laboratory parameters that indicate HIV disease progression. Providers who care for HIV-infected patients need to consider these parameters to establish an appropriate and flexible treatment plan based on changes in the patient's medical status.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Characterization of long-term survivors of acquired immunodeficiency syndrome. The Long-term Survivor Collaborative Study Group.

Of 4,073 reported patients diagnosed with AIDS from 1978 through 1983, 821 (20%) were not reported to be dead by January 1987. Of these apparent long-term survivors, 780 (95%) were reported from 14 states or from local areas where collaborating health departments conducted special follow-up investigations: 119 (15%) were found to be alive, 475 (61%) were dead, and 186 (24%) were lost to follow-up. Health departments obtained consent to collect additional clinical and laboratory information on 48 of the living patients. Six (13%) had no laboratory evidence specific for human immunodeficiency virus (HIV) infection (antibody, antigen, viral isolation, or polymerase chain reaction assay); 41 (85%) had a positive result on at least one test; and one was not tested. Of the 41 infected patients, 25 (61%) had Kaposi's sarcoma (KS) and two (5%) had Pneumocystis carinii pneumonia as the only AIDS-indicative disease; the remainder had multiple diseases. CD4+ cell counts were low (less than 30% of total T lymphocytes) by the time of enrollment in 34 (87%) of 39 patients tested. When enrolled survivors with KS were compared with KS patients who had died within 2 years after AIDS diagnosis, survivors were less likely to have had other diseases in addition to KS than were nonsurvivors (31% versus 51%). While overall mortality by 1987 for patients diagnosed in 1978-83 was high (92-96%), a small number have survived and were doing relatively well clinically, despite evidence of continued CD4+ cell depression.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Long-term survivors: thriving with human immunodeficiency virus/acquired immunodeficiency syndrome.

The lack of a medical cure for human immunodeficiency virus infection and acquired immunodeficiency syndrome has resulted in growing interest in those infected individuals who seem to have longer than expected life spans, a more satisfying and sometimes improved quality of life, and in some cases no progression of immune deterioration. Factors involving genetic predisposition, immune function, and particular psychosocial qualities, such as social affiliations, internal resources, and coping with affective responses, are being studied. Nursing's evolving role in relation to this hopeful development is explored. More research in this area is needed, particularly among those hardest hit in the second wave of the epidemic: women, children, intravenous drug users, and people of color.

Adaptation, Psychological↗
PubMed1991

A prospective study of infants of human immunodeficiency virus seropositive and seronegative women with a history of intravenous drug use or of intravenous drug-using sex partners, in the Bronx, New York City.

A prospective study was conducted in the Bronx, New York, of 70 infants of human immunodeficiency virus (HIV)-infected (n = 33) and uninfected (n = 37) mothers who had a history of intravenous drug use or of intravenous drug-using sex partners. Infants were observed from birth to a median age of 23 months (range 3 to 54 months). HIV infection was confirmed in seven infants (21%) of seropositive mothers; six developed HIV disease, with symptoms observed in the first year. Of these, three died (3, 9, and 36 months) of HIV-related causes; 3 of 4 survivors were greater than 25 months of age. HIV symptoms preceded or were concurrent with abnormalities in T-lymphocyte subsets; postneonatal polymerase chain reaction confirmed HIV infection in five infants with symptoms and one without symptoms. Among infants of seropositive mothers, seven without laboratory evidence of HIV (including polymerase chain reaction) had findings suggestive of HIV infection, including persistent generalized lymphadenopathy, hepatosplenomegaly, oral candidiasis, parotitis, and inverted T-lymphocyte ratios. These findings were not observed in infants of seronegative mothers. Although the presence of HIV proviral sequences was associated with HIV disease, the observation of indeterminate symptoms in at-risk infants indicates the importance of long-term clinical follow-up to exclude HIV infection. Disease manifestations in comparable infants of seronegative mothers are important for assessment of the impact of maternal drug use, development of specific clinical criteria for early diagnosis of HIV and eligibility for antiretroviral therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Neonatal disease induced by SIV infection of the rhesus monkey (Macaca mulatta).

Seven 72-hr-old Indian origin rhesus monkeys (Macaca mulatta) were inoculated with 10 animal ID50 of SIV/DeltaB670. Nine age-matched animals were used as uninoculated controls. All seven inoculated animals became infected as verified by viral isolation and SIV p26 antigenemia. Five of seven infected animals died within a mean of 31 days (range, 26-41 days), with high levels of antigenemia beginning 1-2 weeks postinoculation (PI) that persisted until death. Absolute lymphocyte numbers were within normal limits in all animals in both groups throughout the study. Inoculated animals that died within a mean of 31 days (short-term survivors) had significantly lower numbers of CD4+CD29+ (helper/inducer) lymphocytes than did long-term surviving inoculated animals through 3 weeks PI. Numbers of CD4+ lymphocytes were no different when controls were compared to all inoculated animals through 4-5 weeks PI. The two inoculated animals surviving 216 and 423 days PI (long-term survivors) did demonstrate declining CD4+ cells, but only late in disease. CD8+ lymphocytes were significantly lower in short-term survivors when compared to long-term survivors through 5 weeks PI. Antibody production against SIV viral proteins was detected only in the long-term survivors and was similar to results from past studies in juveniles. Clinical signs in the inoculated group were consistent with those seen in past studies on older animals. Persistent bacterial infections, primarily of the GI and respiratory tracts, were seen in the infected group. Aside from the lack of some opportunistic infections such as cytomegalovirus (CMV) and Pneumocystis carinii, necropsy findings were not different when compared to past studies on juvenile animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗