Human immunodeficiency virus infection in pregnancy

The incidence and prevalence of human immunodeficiency virus (HIV) infection in women of child-bearing age continue to increase both internationally and in Canada. The care of HIV-infected pregnant women is complex, and multiple issues must be addressed, including the current and future health of the woman, minimization of the risk of maternal-infant HIV transmission, and maintenance of the well-being of the fetus and neonate. Vertical transmission of HIV can occur in utero, intrapartum and postpartum, but current evidence suggests that the majority of transmission occurs toward end of term, or during labour and delivery. Several maternal and obstetrical factors influence transmission rates, which can be reduced by optimal medical and obstetrical care. Zidovudine therapy has been demonstrated to reduce maternal-infant transmission significantly, but several issues, including the short and long term safety of antiretrovirals and the optimal use of combination antiretroviral therapy in pregnancy, remain to be defined. It is essential that health care workers providing care to these women fully understand the natural history of HIV disease in pregnancy, the factors that affect vertical transmission and the management issues during pregnancy. Close collaboration among a multidisciplinary team of knowledgeable health professionals and, most importantly, the woman herself can improve both maternal and infant outcomes.     

Human immunodeficiency virus infection in tuberculosis patients

Human immunodeficiency virus (HIV) serology was performed in non-Asian-born patients 18-65 years old with newly diagnosed tuberculosis at a county tuberculosis clinic, and demographic and clinical features of HIV-seropositive and HIV-seronegative patients were compared. Sixty of 128 eligible patients agreed to participate, of whom 17 (28%) were seropositive. Risk of HIV was associated with homosexual contact, intravenous drug use, or both; however, 4 (24%) of the 17 seropositives denied risk behaviors. Significantly more blacks (48%) than whites (10%) or Latinos (20%) were HIV-seropositive (P less than .01). Site of disease, tuberculin reactivity, response to therapy, drug toxicity, and relapse did not differ significantly between groups. HIV-seropositive patients had significantly lower median CD4+ cell counts (326/mm3, range 23-742/mm3, vs. 929/mm3, range 145-2962/mm3, P less than .0005) and median CD4+:CD8+ ratios (0.50, range 0.14-1.07 vs. 1.54, range 0.35-4.36, P less than .0001). HIV infection is associated with clinically typical tuberculosis and HIV screening of tuberculosis patients is recommended in areas where HIV is endemic.     

Human immunodeficiency virus and respiratory infection

Pulmonary disease remains a major problem for the 33 million individuals who are thought to be infected with human immunodeficiency virus (HIV) worldwide. Respiratory infections are responsible for a large number of the 2 million deaths that occur each year in association with HIV disease. In countries where the majority of the population can access highly active antiretroviral therapy, morbidity and mortality rates have been cut by up to 80%. This has allowed the withdrawal of specific opportunistic infection prophylaxis when immune restoration is deemed to be adequate. Recommendations have been published concerning Pneumocystis carinii prophylaxis. This year has also seen further reports of drug-resistant isolates of Pneumocystis carinii. The clinical relevance of this is still debated. Tuberculosis remains a global problem. The complexity of the interactions between specific anti-HIV and anti-tuberculous treatment have been highlighted. In the developing world, the importance of immunization and prophylaxis (against bacteria and mycobacteria) have recently been further defined in a number of studies.     

Meningococcal infection in patients with the human immunodeficiency virus and acquired immunodeficiency syndrome

Meningococcal infection is believed to be rare in HIV-positive individuals. We present 2 cases from our reference caseload within the last 10 years.     

Human immunodeficiency virus and acquired immunodeficiency syndrome: correlation but not causation

AIDS is an acquired immunodeficiency syndrome defined by a severe depletion of T cells and over 20 conventional degenerative and neoplastic diseases. In the U.S. and Europe, AIDS correlates to 95% with risk factors, such as about 8 years of promiscuous male homosexuality, intravenous drug use, or hemophilia. Since AIDS also correlates with antibody to a retrovirus, confirmed in about 40% of American cases, it has been hypothesized that this virus causes AIDS by killing T cells. Consequently, the virus was termed human immunodeficiency virus (HIV), and antibody to HIV became part of the definition of AIDS. The hypothesis that HIV causes AIDS is examined in terms of Koch's postulates and epidemiological, biochemical, genetic, and evolutionary conditions of viral pathology. HIV does not fulfill Koch's postulates: (i) free virus is not detectable in most cases of AIDS; (ii) virus can only be isolated by reactivating virus in vitro from a few latently infected lymphocytes among millions of uninfected ones; (iii) pure HIV does not cause AIDS upon experimental infection of chimpanzees or accidental infection of healthy humans. Further, HIV violates classical conditions of viral pathology. (i) Epidemiological surveys indicate that the annual incidence of AIDS among antibody-positive persons varies from nearly 0 to over 10%, depending critically on nonviral risk factors. (ii) HIV is expressed in less than or equal to 1 of every 10(4) T cells it supposedly kills in AIDS, whereas about 5% of all T cells are regenerated during the 2 days it takes the virus to infect a cell. (iii) If HIV were the cause of AIDS, it would be the first virus to cause a disease only after the onset of antiviral immunity, as detected by a positive "AIDS test." (iv) AIDS follows the onset of antiviral immunity only after long and unpredictable asymptomatic intervals averaging 8 years, although HIV replicates within 1 to 2 days and induces immunity within 1 to 2 months. (v) HIV supposedly causes AIDS by killing T cells, although retroviruses can only replicate in viable cells. In fact, infected T cells grown in culture continue to divide. (vi) HIV is isogenic with all other retroviruses and does not express a late, AIDS-specific gene. (vii) If HIV were to cause AIDS, it would have a paradoxical, country-specific pathology, causing over 90% Pneumocystis pneumonia and Kaposi sarcoma in the U.S. but over 90% slim disease, fever, and diarrhea in Africa.(viii) It is highly improbable that within the last few years two viruses (HIV-1 and HIV-2) that are only 40% sequence-related would have evolved that could both cause the newly defined syndrome AIDS. Also, viruses are improbable that kill their only natural host with efficiencies of 50-100%, as is claimed for HIVs. It is concluded that HIV is not sufficient for AIDS and that it may not even be necessary for AIDS because its activity is just as low in symptomatic carriers as in asymptomatic carriers. The correlation between antibody to HIV and AIDS does not prove causation, because otherwise indistinguishable diseases are now set apart only on the basis of this antibody. I propose that AIDS is not a contagious syndrome caused by one conventional virus or microbe. No such virus or microbe would require almost a decade to cause primary disease, nor could it cause the diverse collection of AIDS diseases. Neither would its host range be as selective as that of AIDS, nor could it survive if it were as inefficiently transmitted as AIDS. Since AIDS is defined by new combinations of conventional diseases, it may be caused by new combinations of conventional pathogens, including acute viral or microbial infections and chronic drug use and malnutrition. The long and unpredictable intervals between infection with HIV and AIDS would then reflect the thresholds for these pathogenic factors to cause AIDS diseases, instead of an unlikely mechanism of HIV pathogenesis.     

Human immunodeficiency virus infection and the liver

Liver disease in human immunodeficiency virus(HIV)-infected individuals encompasses the spectrum from abnormal liver function tests,liver decompensation,with and without evidence of cirrhosis on biopsy,to non-alcoholic liver disease and its more severe form,non-alcoholic steatohepatitis and hepatocellular cancer.HIV can infect multiple cells in the liver,leading to enhanced intrahepatic apoptosis,activation and fibrosis.HIV can also alter gastro-intestinal tract permeability,leading to increased levels of circulating lipopolysaccharide that may have an impact on liver function.This review focuses on recent changes in the epidemiology,pathogenesis and clinical presentation of liver disease in HIV-infected patients,in the absence of co-infection with hepatitis B virus or hepatitis C virus,with a specific focus on issues relevant to low and middle income countries.     

Human immunodeficiency virus infection and renal failure

Renal manifestations are an important component of HIV disease. Renal disease significantly contributes to morbidity and mortality in patients with HIV. Great progress has been made in identifying specific glomerular lesions and its pathogenesis. Newer antiretroviral agents offer great promise in preventing renal disease and also in patients with established HIVAN. Survival of patients with HIV and ESRD (irrespective of cause) who are receiving RRT continues to improve over the years. Acute reversible renal failure, a preventable complication, is also declining in hospitalized HIV patients. More and more physicians, who in the past were reluctant to care for patients with HIV and renal failure because of grim prognosis, are now becoming familiar with the renal sequelae and are encouraged by recent favorable results. As knowledge about viruses is expanding, the proper use of newer highly effective antiretroviral and other agents in complicated patients should further improve both the survival and quality of life in patients with HIV infection and renal disease.     

Human immunodeficiency virus infection and the intestine

HIV is a retrovirus infecting CD4-positive cells causing profound immunosuppression, eventually clinically manifest as AIDS. The cells principally infected by HIV are T4 lymphocytes (helper) and macrophages. The eventual loss of helper cell function is the prime reason for immunodeficiency which renders the individual susceptible to opportunistic infections. HIV infection was first described in male homosexuals. However, the trend now is for seroprevalence to rise rapidly in intravenous drug abusers in the West. In addition, African AIDS is thought to be almost exclusively heterosexual in nature, a paradox which is not yet fully explained in comparison with the relatively low but increasing incidence in heterosexuals in the Western world. Virtually every organ system in the body can be affected clinically during the course of HIV infection. The gastrointestinal tract is a major target, and the physiological sequelae are an important cause of morbidity and mortality. The pathophysiology of intestinal infection is not yet fully understood, however two main mechanisms have been postulated. The first is reduced intestinal immunity resulting in chronic opportunistic infections, which themselves caused altered intestinal function. The second is that HIV itself affects the intestinal mucosa, causing malfunction. The mechanisms by which the latter occurs are controversial but may result from either direct infection of mucosal epithelial cells or macrophages within the mucosa. Reports have documented the presence of HIV genome in both epithelial argentachromaffin cells and macrophages. In addition, profound degeneration of intrinsic jejunal autonomic neurones has been demonstrated, but the functional significance of such denervation is as yet unknown. The clinical stage of HIV infection at which intestinal mucosal immunity fails is by definition when opportunistic infection occurs (that is, clinical progression to stage IV disease), namely AIDS, however a detailed knowledge of the mechanisms of intestinal immune failure are lacking.     

Human immunodeficiency virus infection in patients with leukemia

Eighteen human immunodeficiency virus (HIV)-seropositive patients were found among 211 previously treated adult patients with a variety of leukemias who had been multiply transfused before April 1985. Patients known to be homosexual or intravenous drug users were excluded from this study. The spouse of one HIV-seropositive patient became HIV infected and subsequently developed the acquired immune deficiency syndrome. Patients with leukemia who were multiply transfused before the availability of screening of blood products for HIV antibody should be counseled regarding their individual risks of HIV infection and the risk to sexual contacts.     

Human immunodeficiency virus infection in systemic lupus erythematosus

This report describes a female patient with systemic lupus erythematosus (SLE) who was infected with the human immunodeficiency virus (HIV). Using stored serum, the precise timing of HIV seroconversion was determined and the early effects of HIV infection on SLE examined. This infection resulted in clinical improvement and the disappearance of autoantibody production. A literature review of the association between HIV and SLE is provided.     

Human immunodeficiency virus infection of megakaryocytic cells

The human immunodeficiency virus (HIV) is capable of infecting certain cells of hematopoietic lineage, particularly monocyte-macrophages and T lymphocytes. Recently, the possibility that cells of megakaryocytic lineage are susceptible to HIV infection has been raised. We have characterized infection of the permanent megakaryocytic cell line CMK by HIV in vitro. CMK cells were easily infected by HIV type 2 (HIV-2), producing significant amounts of virus in culture. Infection appeared to be mediated by the CD4 surface antigen on CMK cells. Three different strains of HIV-1 were able to minimally infect CMK cells, suggesting there may be isolates of HIV tropic for megakaryocytes. Infection of CMK cells led to downregulation of the CD4 surface antigen but no discernable change in expression of megakaryocyte-associated proteins glycoprotein Ib and glycoprotein IIb/IIIa. These observations support the likelihood that megakaryocytes are susceptible to HIV infection, and cell lines of megakaryocytic origin may provide a useful model to study effects of the retrovirus on megakaryocyte function.     

Septic arthritis in patients with acquired immunodeficiency syndrome with human immunodeficiency virus infection.

We have evaluated the presence and characteristics of septic arthritis in intravenous (iv) drug users with human immunodeficiency virus (HIV) infection. Sixteen patients with both HIV infection and septic arthritis were studied and compared with 5 patients with septic arthritis but no HIV infection. Clinical profile, laboratory findings at the time of onset, localization, causative organisms, mean hospitalization time and presence of complications were the same in HIV positive and HIV negative patients. Staphylococcus aureus was the most commonly isolated organism in both groups. We conclude that septic arthritis in HIV infected iv drug users is not uncommon, it is produced by the same organisms and presents similar characteristics to the ones found in iv drug users without HIV infection. Therefore, the presence of HIV infection does not appear to modify the characteristics of septic arthritis.     

Human immunodeficiency virus infection in the Republic of Panama

Thirty-one documented acquired immune deficiency syndrome (AIDS) cases occurred in Panama during 1984-1987. Twenty-three (74%) patients were homosexual males and all but 2 patients recognized prior to June 1987 have died. To identify risk factors for human immunodeficiency virus infection, 287 male homosexual residents of Panama City were enrolled in a cross-sectional study. Nine had human immunodeficiency virus (HIV) antibody. Travel to the United States, homosexual relations with United States nationals in Panama, and sexual contacts in Panamanian clubs and bars were associated with human immunodeficiency virus infection by logistic regression analysis. Number of different male sex partners per year was identified but did not enter the logistic model at a significant level. To estimate seroprevalence in other high risk populations, 183 Panama City female prostitutes and 55 homosexual males from the rural Azuero peninsula were screened; none were seropositive. Eighty-four percent of Panamanian hemophiliacs had antibody; infection was related to factor VIII transfusions. Two of 182 sickle cell anemia patients and 15 of 7,720 volunteer blood donors were positive.