AIDS epidemiology: inconsistencies with human immunodeficiency virus and with infectious disease.

The newly defined syndrome AIDS includes 25 unrelated parasitic, neoplastic, and noninfectious indicator diseases. Based on epidemiological correlations, the syndrome is thought to be due to a new, sexually or parenterally transmitted retrovirus termed human immunodeficiency virus (HIV). The following epidemiological data conflict with this hypothesis. (i) Noncorrelations exist between HIV and AIDS; for example, the AIDS risks of infected subjects vary greater than 10-fold with their gender or country. Abnormal health risks that are never controlled as independent AIDS causes by AIDS statistics, such as drug addiction and hemophilia, correlate directly with an abnormal incidence of AIDS diseases. Above all, the AIDS diseases occur in all risk groups in the absence of HIV. (ii) American AIDS is incompatible with infectious disease, because it is almost exclusively restricted to males (91%), because if it occurs, then only on average 10 years after transfusion of HIV, because specific AIDS diseases are not transmissible among different risk groups, and because unlike a new infectious disease, AIDS has not spread exponentially since the AIDS test was established and AIDS received its current definition in 1987. (iii) Epidemiological evidence indicates that HIV is a long-established, perinatally transmitted retrovirus. HIV acts as a marker for American AIDS risks, because it is rare and not transmissible by horizontal contacts other than frequent transfusions, intravenous drugs, and repeated or promiscuous sex. It is concluded that American AIDS is not infectious, and suggested that unidentified, mostly noninfectious pathogens cause AIDS.     

The human immunodeficiency virus and its pathogenesis

HIV is a lentivirus that infects many tissues of the body, including the cells of the brain, the hematopoietic system, and the bowel epithelium. Its spread is mediated by virus-infected cells. Control of HIV depends on a strong host immune response against virus-infected cells, either through suppression of virus release or through killing of the virus-infected cells. Present studies are directed at understanding mechanisms by which effective antiviral therapy and a vaccine can be developed.     

The management of early human immunodeficiency virus infection

The outcome of treatment in patients with early asymptomatic HIV disease has recently improved. Clinical trials with zidovudine have demonstrated efficacy and greatly reduced toxicity when the drug is used in asymptomatic HIV-infected persons who have fewer than 500 CD4+ cells/mm3, and resistance to this drug in these patients is less frequent and severe. Also, the optimum dosage of zidovudine is less than previously believed, probably in the range of 500-600 mg daily given in oral divided doses. The use of antibiotics to prevent Pneumocystis carinii pneumonia is also of clear value in HIV-infected asymptomatic or symptomatic persons with fewer than 200 CD4+ cells/mm3. Oral regimens such as trimethoprim/sulfamethoxazole or dapsone alone appear to be effective and are gaining preference over aerosolized pentamidine that is considerably more expensive. Together these medical advances argue for the encouragement of voluntary HIV testing to enable early diagnosis and, hence, optimum medical monitoring and appropriate intervention. These issues and recommendations for laboratory and clinical monitoring will be provided in this review.     

A review of the epidemiology, prevention and treatment of human immunodeficiency virus infection in Nigeria.

In order to amalgamate research findings on HIV/AIDS in Nigeria as well as the trend of the infection in a concise manner, we reviewed published articles on the HIV/AIDS situation in Nigeria. We categorized this review into several subheadings. The HIV prevalence rate has continued to rise steadily from less than 0.1% in 1987, to 5.8% in 2001, with a slight decrease in 2003 to 5.0%. Although the knowledge about HIV and its mode of transmission is widespread, it is however disheartening to note that this did not result into appreciable attitudinal change and behavior modification among Nigerians. Both HIV-1 and HIV-2 have been identified in Nigeria, with HIV-1 being the predominant type. Furthermore, several subtypes like subtypes A, B, C, G and J have been identified in Nigeria, with several recombinant forms like the CRF02_AG; the major ones being A, G and CRF02_AG. HIV-infected patients in Nigeria are also co-infected with other viral and bacterial infections, the commonly reported ones being co infections with hepatitis B and C. Although treatment of infected patients has increased recently, more effort is needed, especially in the area of patients monitoring, to maximize the benefits of ART in Nigeria. Finally, Nigeria has made appreciable efforts in vaccine development and candidate HIV DNA vaccines have been developed utilizing the sequences from predominant subtypes, and these candidates have been shown to be immunogenic in animal models. It is therefore clear that only the integration of prevention and antiretroviral research programmes into a coherent programme that is needed to address the public health needs that HIV/AIDS crisis represents for Nigeria.     

The natural history of human immunodeficiency virus infection

Although much is known about the natural history of HIV infection, many issues remain unresolved and require additional study. At least four major questions require further investigation. (1) Current data suggest that most HIV-infected persons will eventually develop AIDS. The proportion of all infected persons who will eventually develop AIDS, as well as the average and maximum incubation periods, have not yet been conclusively defined. (2) Certain clinical signs (such as oral candidiasis) or laboratory test results (such as a depressed T4 count) may indicate a poorer prognosis. However, the predictive value of such indicators for a specific patient and in an individual situation varies. Combinations of clinical and laboratory data may help refine estimates of the likelihood of developing AIDS or other HIV-related diseases. (3) Why some HIV-infected persons develop disease and others do not is not completely understood. The role of cofactors for disease progression needs additional investigation. There may be no one universal cofactor for progression but, rather, various agents that cause immune stimulation and reactivation of latent HIV. Therefore, exposure to a variety of infectious or environmental agents (such as through sexually transmitted diseases or injection of iv drugs) may accelerate progression to disease in HIV-infected persons. (4) It is not established whether antiviral agents will prevent or reduce the likelihood of disease progression in asymptomatic HIV-infected persons. If beneficial, should they be given to all HIV-infected persons or only to those whose clinical and laboratory evaluation suggests an increased likelihood of progression? Given these uncertainties, how should the physician or other health care worker evaluate, treat, and counsel the HIV-infected patient? Such patients should receive a comprehensive medical evaluation for both diagnostic and staging purposes; the details of such an evaluation are beyond the scope of this review and have been well described. A few brief points, however, should be emphasized.(ABSTRACT TRUNCATED AT 250 WORDS)     

The rheumatic manifestations of infection with the human immunodeficiency virus

The recognized clinical spectrum of disease associated with HIV infection is rapidly expanding and now includes a variety of rheumatic syndromes. The laboratory features of HIV infection closely resemble those found in many connective tissue diseases and thus alter the predictive value of these tests in the evaluation of both types of conditions. In addition to the laboratory similarities, there are also increasing numbers of clinical reports of HIV-infected individuals who develop syndromes either resembling classic idiopathic rheumatic diseases such as SS, polymyositis, or SLE, or newly recognized illnesses that fall under the clinical domain of the rheumatologist (ie, HIV-associated vasculitis and arthritis). It is vital that clinicians recognize these new illnesses because there are important differences in prognosis and management between these and their idiopathic counterparts. Research is urgently needed for better definition of these syndromes and their pathogenesis, natural history, and optimal therapies.     

Molecular epidemiology of human immunodeficiency virus type 1 and hepatitis C virus in former blood donors in central China

The prevalence of hepatitis C virus (HCV) among human immunodeficiency virus (HIV-1)-positive former blood donors (FBDs) in Hubei province, central China, and the subtypes of these two viruses are identified. HIV-1-positive specimens were collected from FBDs, transfusion recipients, and their sexual partners in Hubei province, central China. The prevalence of HCV in HIV-1-positive FBDs was 78.6%. The dominant circulating HIV-1 subtype of FBDs was subtype B' (Thai-B); one belonged to U.S.-European subtype B. HCV genotypes 2a (78.6%) and 1b (21.4%) were detected. No recombinant form of HIV-1 was identified. Non-B' subtypes occurring among FBDs indicate the complexity of the HIV-1 prevalence in central China, where HIV is beginning to spread into the general population.     

人类免疫缺陷病毒与重叠丙型肝炎病毒感染者免疫指标比较

目的 分析HIV/HCV重叠感染人群与HIV单独感染人群治疗前临床特征及免疫功能的差异,探讨其可能的影响因素.方法 以HIV/HCV重叠感染患者59例、HIV单独感染患者38例为研究对象,取患者治疗前外周血,检测其肝功能、血常规、外周血T细胞亚群(CD4+、CD8+)及HIV、HCV病毒载量,酶联免疫斑点法(ELISPOT)检测HIV特异性细胞毒性T淋巴细胞(CTL)的数量和功能.结果 HIV/HCV重叠感染率达60.8%.重叠感染组ALT、AST均明显高于HIV组(49.8 U/L比23.6 U/L,49.1 U/L比32.3 U/L,P值分别为0.000、0.013);重叠感染组PLT明显低于HIV组[(167.3±59.2)×109/L比(198.0±63.9)×109/L,P=0.040].外周血T细胞亚群检测结果两组间差异无统计学意义.重叠感染组HIV RNA定量为(4.046±0.541)lOglo拷贝/mL,低于HIV组的(4.394±0.507)log10拷贝/mL(P=0.018).重叠感染组对HIV-Gag全序列肽段的阳性孔斑点数(平均秩次30.85)较HIV组(平均秩次44.34)低,阳性孔数(4.60±5.52)低于HIV组(6.24±6.93),但两组比较差异无统计学意义.重叠感染组Alb与HCV病毒载量呈负相关(r=-0.540),CD4+与PLT呈正相关(P=0.000).结论 单采血浆感染HIV患者中,有较高的HIV/HCV重叠感染率和较低的细胞免疫功能.     

Mucosal transmission of human immunodeficiency virus

Since the beginning of the AIDS pandemic, and following the discovery of the human immunodeficiency virus (HIV) as the etiological agent of the disease, it was clear that the virus gains access to the human host predominantly through the mucosal tissue after sexual exposure. As a consequence, the female genital tract (vaginal and cervical), as well as the rectal, penile, and oral mucosae have been extensively studied over the last thirty years towards a better understanding of--and to develop strategies to prevent--sexual HIV transmission. This review seeks to describe the biology of the events leading to HIV infection through the human mucosa and introduce some of the approaches attempted to prevent the sexual transmission of HIV.     

Rheumatic manifestations of human immunodeficiency virus

Since July 1983, various rheumatic, musculoskeletal, or other immune disorders characterized by dysregulation have been associated with HIV and AIDS. Infections occur, but with a lower frequency than expected in a patient population with a disorder primarily characterized by significant cellular immune deficiencies. Reactive arthritis, psoriatic arthritis, acute nonspecific arthritis, Sjögren syndrome, and inflammatory myositis have been reported. The initial reports of "acute painful joints," however, have not maintained prominence in the literature. A review of the literature over the past several years has reinforced the perception that the initial excitement over a possible association between HIV and AIDS and rheumatic or definable autoimmune disorders remains limited to a small segment of illnesses dominated by the reactive arthritidies.     

Quantifying the infectivity of human immunodeficiency virus.

We have developed a mathematical model that quantifies lymphocyte infection by human immunodeficiency virus (HIV) and lymphocyte protection by blocking agents such as soluble CD4. We use this model to suggest standardized parameters for quantifying viral infectivity and to suggest techniques for calculating these parameters from well-mixed infectivity assays. We discuss the implications of the model for our understanding of the infectious process and virulence of HIV in vivo.     

Management of the coinfected patient: human immunodeficiency virus/hepatitis B and human immunodeficiency virus/hepatitis C

Deaths from liver disease have increased in persons infected with human immunodeficiency virus (HIV) because of coinfection with chronic hepatitis B and C; consequently, all HIV-infected patients should be screened for hepatitis B and C, and all those susceptible should be vaccinated for hepatitis B. Hepatitis A vaccination is indicated for susceptible coinfected patients. It is also important to stress other means of preventing the transmission of hepatitis, such as safe sex and avoidance of blood exposures. Three oral agents, lamivudine, adefovir, and tenofovir, are active against hepatitis B infection. The need for highly active antiretroviral therapy and hepatitis B therapy should be addressed in a coordinated fashion, since two of these agents are active against both HIV and hepatitis B virus. Oral combination therapy for hepatitis B infection looks promising but needs further study. Combination therapy for chronic hepatitis C with pegylated interferon plus ribavirin is the most effective available therapy and the current standard of care. Prior to therapy, patients should be evaluated for contraindications to therapy. During treatment, they should be closely monitored for adverse events.     

The epidemiology and prevention of the acquired immunodeficiency syndrome

The incidence of the acquired immunodeficiency syndrome (AIDS) has continued to increase worldwide. From June 1981 to September 1985, 12 932 cases have been diagnosed and reported in the United States; this number is expected to double during the next year. The incubation period is long and few persons infected with human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV) have AIDS diagnosed within 2 to 5 years of infection. The widespread use of HTLV-III/LAV serologic tests to screen donated blood and plasma, the continued deferral of donors from groups with an increased incidence of AIDS, and the use of heat-treated clotting factor concentrates should help prevent HTLV-III/LAV transmission through blood and blood products. Preventing transmission among sexual partners, among intravenous drug users, and from infected mothers to newborns will continue to be difficult without a vaccine, specific antiviral therapy, or both. Risk reduction strategies should involve community groups to provide accurate information and influence behaviors that lead to transmission of the virus.     

Impact of the human immunodeficiency virus on the epidemiology of tuberculosis in area 15 of the Valencian community in Spain.

SETTING: Area 15 in Valencia. OBJECTIVES: To describe the epidemiology (1987-2001) of tuberculosis (TB) in human immunodeficiency virus (HIV) patients. METHODS: Study of annual incidence, age distribution, excess cases attributed to HIV, etiological risk fraction (ERF), population attributable fraction (PAF) and f factor. RESULTS: Of 476 cases diagnosed, 459 were TB, 16 environmental and one mixed; 76% of environmental cases were HIV-positive (P < 0.001). There was a mean annual TB incidence of 24.6/100000, with an annual reduction of 4%. Seventy-three patients were HIV coinfected (16%) (mean incidence 3834/100 000 seropositives). The principal risk factor was drug use (59%) for HIV+ and contact with TB for HIV-. We found no difference in pulmonary or extra-pulmonary location between groups, contrary to mixed cases (P < 0.001). In HIV+ there was a lower frequency of infiltrates (P < 0.001) and cavitation (P < 0.01), and a higher frequency of adenitis (P < 0.001), miliary or nodular pattern and normal X-ray (P < 0.001). Seropositives had a 174 times higher probability of developing TB. The mean ERF attributed to HIV was 99%, the PAF was 16% and the f factor was 1.19. Highly active antiretroviral therapy (HAART) reduced the risk of TB in HIV+ by 80%. CONCLUSIONS: TB has continued its decline, although HIV generated an excess of cases in the 1990s. HAART has reduced the TB risk in HIV+ and possibly the overall rate of TB.