Background: Hematological abnormalities are a common complication of HIV infection. These abnormalities increase as the disease advances. Bone marrow abnormalities occur in all stages of HIV infection.

HIV infection increases the oxidative stress process, and antiretroviral combination therapy increases protein oxidation and preexistent oxidative stress. The latter induces production of reactive oxygen species. Lipid peroxidation (LPO) is a means of determining oxidative stress. There is also a deficiency of glutathione in HIV infection. Persistent oxidative load leads to an accelerated rate of consumption of glutathione (GSH). This study measured LPO and GSH levels in plasma of HIV-infected individuals with or without therapy and compared these with healthy controls. One hundred HIV-infected individuals and 30 healthy controls were included in the study. LPO and GSH levels were measured in plasma according to previously described methods. The mean level of LPO in HIV-infected individuals was 0.7 +/- 0.1 micromol/ml (range, 0.5-0.9 micromol/ml), whereas the mean LPO level in controls was 0.3 +/- 0.1 micromol/ml (range, 0.2-0.4 micromol/ml). The mean LPO levels were significantly higher in HIV-infected individuals as compared to healthy controls (p value <0.0001). The mean GSH level in HIV-infected individuals was 0.06 +/- 0.01 micromol/ml (range, 0.03-0.08). The mean GSH level in healthy controls was 0.09 +/- 0.01 micromol/ml (range, 0.05-0.1). The mean glutathione level in HIV-infected individuals was significantly lower in compared to healthy controls (p value < 0.0001). There was a significant positive correlation between absolute CD4 cells and GSH levels (rho = 0.182, p = 0.045). There is increased oxidative stress in HIV-infected patients. Whether supplementation with antioxidants will reduce this oxidative stress is still unknown.

HIV infection is associated with a number of opportunistic infections and malignancies frequently involving the lymph nodes. Lymphadenopathy may occur at any stage of HIV infection. We aimed to determine the utility of fine-needle aspiration cytology in evaluating the causes of lymphadenopathy in HIV-infected individuals. Three hundred HIV-infected individuals with lymphadenopathy were included in the study. Fine-needle aspiration (FNA) was performed on peripheral or deep-seated lymph nodes. The material was used for cytological examination using May-Grunwald-Giemsa and haematoxylin and eosin staining. Special stains such as modified Ziehl-Neelsen staining for acid-fast bacilli and periodic acid-Schiff staining for fungi were also performed. The mean age of the study group was 35.0 ± 8.0 y (range 13-74 y). The median CD4 count was 152 cells/μl. Out of the 300 FNA reports, acid-fast bacteria were reported in 130 and cytological findings indicating mycobacterial infection in a further 43 patients. Cryptococcosis was reported in 4 individuals, histoplasmosis in 2 and aspergillosis in 1. Reactive hyperplasia was seen in 89 individuals. Lymphoma was noted in 7 individuals and suppurative inflammation in 5. In conclusion, tuberculosis is the predominant cause of lymphadenitis in HIV-infected individuals in India, especially in those with low CD4 cell counts.

Background Government of India is committed to eliminate measles and control rubella/congenital rubella syndrome (CRS) by 2020. In 2016, CRS surveillance was established in five sentinel sites. We analyzed surveillance data to describe the epidemiology of CRS in India. Methodology/Principal findings We used case definitions adapted from the WHO-recommended standards for CRS surveillance. Suspected patients underwent complete clinical examination including cardiovascular system, ophthalmic examination and assessment for hearing impairment. Sera were tested for presence of IgM and IgG antibodies against rubella. Of the 645 suspected CRS patients enrolled during two years, 137 (21.2%) were classified as laboratory confirmed CRS and 8 (1.2%) as congenital rubella infection. The median age of laboratory confirmed CRS infants was 3 months. Common clinical features among laboratory confirmed CRS patients included structural heart defects in 108 (78.8%), one or more eye signs (cataract, glaucoma, pigmentary retinopathy) in 82 (59.9%) and hearing impairment in 51. (38.6%) Thirty-three (24.1%) laboratory confirmed CRS patients died over a period of 2 years. Surveillance met the quality indicators in terms of adequacy of investigation, adequacy of sample collection for serological diagnosis as well as virological confirmation.

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Repeated exposure to human immunodeficiency virus (HIV) does not always result in infection. Understanding the mechanisms that give protection against progressive infection with HIV may help in the development of a vaccine. In order to determine the influence of host genetic factors on HIV resistance, we studied 35 exposed but uninfected (EU) partners of HIV-1 infected individuals for polymorphisms in multiple chemokine and chemokine receptor genes and compared the results with those for 75 HIV-1 seronegative normal healthy controls (HC) and 50 HIV infected controls. There was no association between CCR5-Delta32, CCR2-64I, CX3CR1-280 M, CX3CR1-249I, SDF-3'A, RANTES-28G and RANTES-403A polymorphisms and susceptibility against HIV in our cohort of EU individuals. An increased frequency of SDF-1 3'A and RANTES-403A genotypes was present in EU individuals but the difference was not statistically significant when compared to healthy and HIV infected controls. These observations suggest that mechanisms other than genetic mutations of these genes might be responsible for resistance to HIV infection in these individuals.

Non-protease inhibitor-based antiretroviral therapy (ART) is widely accepted as first-line ART in developing countries. Although reverse transcriptase inhibitor-based regimens have been studied in the peripheral blood, no studies have analyzed alterations in cytokine and chemokine levels, together in peripheral blood and genital secretions. Forty HIV-infected women with CD4 cell counts <200 cells/mm(3), asymptomatic, with no genital tract infection, willing to participate in the study, and adhere to ART were enrolled. Cervicovaginal lavage (CVL) was collected in the mid-cycle phase of menstrual cycle. Patients were initiated with reverse transcriptase-based antiretrovirals. Repeat sampling was performed at 24 weeks. Cytokines and chemokines were measured using ultrasensitive ELISA kits. Viral load declined to undetectable levels in 29 patients in the blood and in 33 cases in the CVL. Proinflammatory cytokines (tumor necrosis factor-alpha [TNF-alpha, interleukin-6 [IL-6], IL-1beta) in the serum and CVL showed a significant decrease in mean levels after therapy. IL-2 levels increased significantly whereas IL-12 and (IFN-gamma decreased in both compartments. Mean levels of IL-4 and IL-10 decreased significantly in the serum. There was direct correlation between serum and CVL levels of IL-2 and IL-10. IL-10 had a negative correlation with CD4% at baseline and 6 months of therapy. Mean levels of all alpha- and beta-chemokines decreased in serum after therapy. In CVL, mean levels of MIP-1alpha, RANTES, and IL-8 reduced and SDF-1alpha increased significantly (P value <0.001). Serum levels of all the cytokines, except IL-2, and all chemokines prior to therapy, were significantly higher than healthy controls. In CVL, mean levels of TNF-alpha, IL-6, IL-1beta, IL-12, IFN-gamma, IL-10, RANTES, and IL-8 were significantly higher, whereas IL-2, MIP-1alpha, and MIP-1beta were significantly lower than healthy controls. The mean levels of proinflammatory cytokines and chemokines significantly decreased in serum and CVL after therapy, possibly due to reduced viral load.

As the developing world increasingly uses generic ART, the clinician must be constantly vigilant for treatment-related adverse events.