Plasma cell endometritis is associated with Chlamydia trachomatis infection.

The presence of plasma cells in endometrial tissue has been linked to Chlamydia trachomatis infection. The aim of our work was to determine the strength of the association between C trachomatis infection and plasma cell endometritis. C trachomatis infection was detected by polymerase chain reaction (PCR) or immunohistochemistry in 5 (24%) of 21 endometrial tissue samples with plasma cell endometritis and in 1 (4%) of 28 tissue samples with no evidence of plasma cell endometritis (P < .02). Patients with plasma cell endometritis were also more likely to have symptoms and signs consistent with upper genital tract chlamydial infection; thus there is an association between endometrial C trachomatis infection and the presence of plasma cells in the endometrium. The histopathologic finding of plasma cell endometritis should encourage further examination of the tissue sample for simultaneous chlamydial infection. Plasmid-based polymerase chain reaction and immunohistochemical staining of paraffin-embedded samples are useful methods for detecting C trachomatis in endometrial tissue.     

Vasculitides associated with HIV infection

The manifestations of human immunodeficiency virus (HIV) infection are protean and vasculitides are one of the less common but nonetheless important consequences. A wide range of vasculitides can be encountered, ranging from vasculitis resulting from specific infective agents to a non-specific vasculitis. Among the infective causes, cytomegalovirus and tuberculosis are probably the most common. A polyarteritis nodosa-like vasculitis with important differences to classic polyarteritis nodosa is also described. Hypersensitivity vasculitis resulting in several patterns of vasculitis and angiocentric immunoproliferative vasculitis are well recognised. As part of the immunocompromise caused by HIV, a granulomatous inflammation involving small arteries and veins of the brain surface and leptomeninges, termed a primary angiitis of the central nervous system, is a rare vasculitis associated with high mortality. A recently described large vessel (aorta, femorals, carotids) vasculopathy resulting in either multiple aneurysm formation or occlusive disease is seen in young adults. An infective agent is not found but aetiologically some of these lesions might be the result of a leucocytoclastic vasculitis of vasa vasora or periadventitial vessels. A final group of non-specific vasculitides not fitting into any of the characteristic patterns described accounts for the residue of vasculitides associated with HIV.     

Risk reduction counseling is associated with decreased HIV transmission-associated behaviors in high-risk Indian heterosexuals

OBJECTIVE: To estimate the incidence of HIV and study the impact of risk-reduction counseling (RRC) in a cohort of people with high-risk behavior for HIV transmission in Chennai, India. DESIGN: Prospective cohort follow-up of 500 HIV-negative people (250 men and 250 women) at increased risk for HIV acquisition in Chennai, India for a maximum of 1 year was conducted. They received RRC at 0, 6, and 12 months. Generalized estimating equation methodology was used to determine the statistical significance of differences reported in behavior between baseline, 6 months, and 12 months. RESULTS: The overall HIV incidence in this cohort was 0.44 per 100 person-years (95% confidence interval: 0.05-1.60). In the course of the study, both male and female participants reported statistically significant decreases in the number of different sexual partners, the number of new partners, and the proportion of sexual encounters with nonprimary partners. Participants who had more than 3 different partners at baseline and/or exchanged money for sex in the 6 months before enrollment demonstrated the greatest reductions in the number of different sexual partners. CONCLUSIONS: Individualized sexual RRC seems to be a useful intervention to reduce risk-taking behavior among at-risk heterosexuals in India.     

Nutritional alterations associated with HIV infection

Nutritional alterations are common in HIV infection. Early studies documented weight loss and protein depletion, a finding associated with body cell mass depletion in untreated patients. The application of highly active antiretroviral therapy has led to a decreased incidence of malnutrition, although altered body fat distribution and metabolic alterations, including hyperlipidemia and insulin resistance, are common sequelae. The development of malnutrition is multifactorial and occurs through changes in caloric intake, nutrient absorption, or energy expenditure. Clinically, malnutrition develops as a result of either starvation or cachexia. Other hormonal and endocrinologic alterations include hypercortisolemia and hypogonadism. The rationale for providing nutritional support to AIDS patients is based upon the assumptions that nutrition status can be improved and that such improvements have clinical benefits. The results of hypercaloric feeding studies, including the use of appetite stimulants, indicate that weight gain is possible but that the weight gained is predominantly fat. In contrast, anabolic agents and resistance training exercise have been shown to promote body cell mass repletion and skeletal muscle gain. Cytokine inhibitors also have been evaluated for the treatment of wasting in HIV infection. Development of combination therapies, preventive therapies, and efficient and cost-effective therapies are current tasks in the field.     

Oral manifestations associated with HIV infection

Oral lesions are among the early signs of HIV infection and can predict progression to AIDS. The lesions commonly associated with the infection include oral candidiasis, herpes simplex infection, oral Kaposi’s sarcoma, oral hairy leukoplakia, parotid gland enlargement, gingival diseases, xerostomia, and recurrent oral ulcerations. The introduction of highly active antiretroviral therapy has changed the epidemiology of some of the oral diseases associated with HIV infection. This review discusses the oral manifestations associated with HIV disease, the change in the pattern of the disease, and some research questions that need more emphasis from the research community.     

Disturbance of the gut-associated lymphoid tissue is associated with disease progression in chronic HIV infection

Why and how HIV makes people sick is highly debated. Recent evidence implicates heightened immune activation due to breakdown of the gastrointestinal barrier as a determining factor of lentiviral pathogenesis. HIV-mediated loss of Th17 cells from the gut-associated lymphoid tissue (GALT) impairs mucosal integrity and innate defense mechanisms against gut microbes. Translocation of microbial products from the gut, in turn, correlates with increased immune activation in chronic HIV infection and may further damage the immune system by increasing viral and activation-induced T cell death, by reducing T cell reconstitution due to tissue scarring, and by impairing the function of other cell types, such as γδ T cells and epithelial cells. Maintaining a healthy GALT may be the key to reducing the pathogenic potential of HIV.     

Human uracil-DNA glycosylase deficiency associated with profoundly impaired immunoglobulin class-switch recombination

Activation-induced cytidine deaminase (AID) is a 'master molecule' in immunoglobulin (Ig) class-switch recombination (CSR) and somatic hypermutation (SHM) generation, AID deficiencies are associated with hyper-IgM phenotypes in humans and mice. We show here that recessive mutations of the gene encoding uracil-DNA glycosylase (UNG) are associated with profound impairment in CSR at a DNA precleavage step and with a partial disturbance of the SHM pattern in three patients with hyper-IgM syndrome. Together with the finding that nuclear UNG expression was induced in activated B cells, these data support a model of CSR and SHM in which AID deaminates cytosine into uracil in targeted DNA (immunoglobulin switch or variable regions), followed by uracil removal by UNG.     

Plasma RNA viral load is not associated with intrapatient quasispecies heterogeneity in HIV-1 infection

Summary. The human immunodeficiency virus type 1 (HIV-1) viral set point has been associated with the rate of disease progression and with the level of HIV-specific immune response. The analysis of the possible association between viral set point and quasispecies heterogeneity has important consequences in the understanding of HIV-1 in vivo evolution. In this study, we analyzed the association between intrapatient viral diversity and RNA viral load in 16 antiretroviral therapy-naïve HIV-1-infected patients at a single time point, during the disease free period. Patients were separated into low and high viral load groups according to plasma RNA values. HIV-1 quasispecies complexity was assessed in the C2-V5 env region. The average intrapatient quasispecies heterogeneity in both groups was not significantly different (t-test, P > 0.05). However, while within the low viral load group both synonymous and non-synonymous mutations contribute to the variation observed, in the heterogeneity observed in the high viral load group there was an increase in the contribution of the non-synonymous mutations. Thus, this study show that although intrapatient quasispecies heterogeneity is not associated with viral set point in HIV-1 infection, some differences exist between the two groups in the pattern of mutation accumulation.     

Laboratory markers associated with progression of HIV infection

Infection with HIV may develop to AIDS at different rates in different individuals, with a spectrum varying from rapid progression to long term non-progression. The variable course of HIV-1 infection causes emotional trauma for the infected person and complicates the design and interpretation of therapeutic trials because of unrecognized differences in prognosis. Thus it is essential to have tests which can accurately assess the stage of infection in an individual, as well as predict its course and monitor its progression. These laboratory tests are very valuable during the period of clinical latency and subsequently supplement various clinical parameters.     

Trunk antagonist co-activation is associated with impaired neuromuscular performance

The goal of this paper was to determine if trunk antagonist activation is associated with impaired neuromuscular performance. To test this theory, we used two methods to impair neuromuscular control: strenuous exertions and fatigue. Force variability (standard deviation of force signal) was assessed for graded isometric trunk exertions (10, 20, 40, 60, 80% of max) in flexion and extension, and at the start and end of a trunk extensor fatiguing trial. Normalized EMG signals for five trunk muscle pairs (RA rectus abdominis, EO external oblique, IO internal oblique, TE thoracic erector spinae, and LE lumbar erector spinae) were collected for each graded exertion, and at the start and end of a trunk extensor fatiguing trial. Force variability increased for more strenuous exertions in both flexion (P < 0.001) and extension (P < 0.001), and after extensor fatigue (P < 0.012). In the flexion direction, both antagonist muscles (TE and LE) increased activation for more strenuous exertions (P < 0.001). In the extension direction, all antagonist muscles except RA increased activation for more strenuous exertions (P < 0.05) and following fatigue (P < 0.01). These data demonstrate a strong relationship between force variability and antagonistic muscle activation, irrespective of where this variability comes from. Such antagonistic co-activation increases trunk stiffness with the possible objective of limiting kinematic disturbances due to greater force variability.     

Peripheral CD4 loss of regulatory T cells is associated with persistent viraemia in chronic HIV infection

Chronic HIV infection is associated with T cell abnormalities and altered effector function. Regulatory T cells (Treg) are CD4+ T cells that play a critical role in regulating the immune system. The impact of regulatory T cells on HIV infection and disease progression may be highly significant. We hypothesize that chronic antigenic stimulation from a persistent, high viraemic state may promote a population of Treg that contributes to HIV-associated immune dysfunction. We evaluated the pattern of Treg in chronically infected, HIV-positive individuals over a course of 6 months. Treg are depleted at a distinct rate from that of absolute CD4 cells and loss of Treg is slower in the presence of viral suppression. In vitro depletion of CD25+ CD4+ cells resulted in increased Gag-specific CD4 and CD8 responses. A significant correlation between ex vivo measurement of Treg and Gag-specific CD4 T cell responses was observed (r=-0 x 41, P=0 x 018) with a trend observed with Gag-specific CD8 T cell responses (P=0 x 07). The impact of HIV infection on the Treg population directly complicates the measured effect of Treg on the immune dysfunction although our data support the important role of Treg on modulating the effector T cell response in chronic infection.     

Electrophysiologic study in peripheral neuropathy associated with HIV infection.

Clinical and electrophysiologic features in 22 patients with HIV infection are reported. Four cases had chronic demyelinating polyneuropathy, two mononeuropathy multiplex, and nine symmetrical sensory-motor polyneuropathy. Seven cases had normal clinical and electromyographic examination. Electrophysiological study had a higher diagnostic yield (68%) than clinical examination (50%) for peripheral neuropathy diagnosis. Thus, peripheral nerve abnormalities are frequent in patients with different stages of HIV infection, although their pathogenesis remains unclear. Symmetrical sensory-motor polyneuropathy is the main type of neuropathy seen in ouvert AIDS, whereas chronic demyelinating polyneuropathy was mainly diagnosed in patients with asymptomatic HIV infection as first manifestation of the disease. Axonal or demyelinating nerve damage was established according to electrophysiological criteria. Frequently a mixture of both lesions was found. Electrophysiologic study is also a good index of neuropathy evolution in HIV infection and to follow-up of nerve abnormalities after treatment.