Does HIV infection alter the incidence or pathology of Helicobacter pylori infection?

Gastrointestinal (GI) discomfort is a common complaint among patients infected with HIV. GI symptoms can be caused by a myriad of factors including but not limited to coinfections, antiretroviral therapy, medications for opportunistic infections, and nutritional status. Some researchers have hypothesized that Helicobacter pylori infection may be more common among HIV-infected patients as a result of immune suppression. An increased incidence of H. pylori infection would contribute to the prevalence of GI complaints in this population. Several epidemiologic studies have examined the relationship between H. pylori infection and HIV. While studies have generally reported conflicting results that may be related to the use of varied study designs, some identifiable patterns can be discerned. It does appear that the incidence of H. pylori infection is lower among patients with AIDS compared to matched HIV-infected and -uninfected controls. This review discusses the various epidemiologic trials that have been conducted in this area and describes the potential physiologic mechanisms to explain these findings. The clinical applicability of these studies as well as limitations are also discussed. A greater number of well-designed and controlled trials are needed before any definitive conclusions regarding these diseases can be made, until such time clinicians should be aware of the potential issues regarding H. pylori screening and management in the context of HIV. Research in this area might also provide information relating to HIV-associated GI changes and the role of these changes in HIV pathogenesis.     

Cancer and HIV infection: any association?

PURPOSE: Morbidity and mortality related to neoplasia are increasing in HIV-infected patients. CURRENT KNOWLEDGE AND KEY-POINTS: The incidence of AIDS opportunistic infections dramatically decreased since the introduction of highly active antiretroviral therapy (HAART). Among AIDS-cancers, the incidences of Kaposi sarcoma and of cerebral lymphoma decreased in a same way than AIDS infections but the incidences of systemic non-Hodgkin lymphoma and of cervical cancer decreased less than the others and remain higher than in the general population. This suggests that other factors than the quantitative immune reconstitution could be implicated. The most recent and large studies have also shown a 1.7 to 3 fold increased risk of developing non-AIDS cancers in HIV-infected patients when compared to the general population without significant impact of HAART on incidence curves. These malignancies include Hodgkin disease, lung, anal, head and neck cancers, hemopathies, and conjunctival cancers. PERSPECTIVES: Epidemiologic survey will help to define priorities in terms of prevention and screening in this specific population and to evaluate interventions which should be systematically proposed (alcohol and tobacco cessation programs, viral coinfection). The own roles of HIV itself and of antiretrovirals as prooncogenic factors need to be assessed.     

Non—AIDS–Defining cancers and HIV infection

With fewer patients now succumbing to infectious complications of AIDS, other HIV-related morbidities such as malignancies have become increasingly important. Apart from Kaposi’s sarcoma, non-Hodgkin’s lymphoma, and cervical cancer, which are considered as AIDS-defining, several additional cancers, referred to as non-AIDS-defining cancers, are also statistically increased in HIV-infected persons. These include Hodgkin’s disease, anal carcinoma, lung cancer, nonmelanomatous skin cancer, and testicular germ cell tumors, among others. However, the types of cancer observed at an increased frequency and the relative risks reported vary widely among studies. Although immunosuppression is consistently associated with an increased risk of AIDS-related malignancies, the role of immunosuppression in the pathogenesis of non-AIDSdefining cancers is controversial. Although data regarding the optimal management of these cancers are lacking, current studies suggest that patients with HIV-associated malignancies should be treated with similar approaches to those of their counterparts in the general population.     

cAMP during HIV infection: friend or foe?

Intracellular levels of cyclic adenosine 3',5'-monophosphate (cAMP) are important regulators of immune cells, partially determining the balance between activation and suppression. In this review, we discuss the mechanisms by which HIV infection increases cAMP levels in T cells, as well as the effect of cAMP on HIV-specific responses and its effect on HIV replication and infection. Results suggest that increased cAMP levels during HIV infection may have a dual and opposite roles. On the one hand, they could have a protective effect by limiting viral replication in infected cells and decreasing viral entry. On the other hand, they could have a detrimental role by reducing HIV-specific antiviral immune responses, thus reducing the clearance of the virus and contributing to T cell dysfunction. Future studies are thus needed to further define the beneficial versus detrimental roles of cAMP, as they could help establish new therapeutic targets to combat HIV replication and/or identify novel ways to boost antiviral immune responses.     

Natural resistance to HIV infection: lessons learned from HIV‐exposed uninfected individuals

We explored potential mechanisms of resistance to human immunodeficiency virus type 1 (HIV‐1) infection in different groups of uninfected individuals exposed by systemic or mucosal routes: intravascular drug users in Vietnam and spouses of HIV‐infected individuals in Cambodia and Central African Republic. Our main findings were reduced susceptibility of peripheral blood mononuclear cells to HIV‐1 infection in vitro, associated with low levels of CD4+ T cell activation in vivo and/or cell restriction of viral replication, and enhanced natural killer cell activity, associated with increased ratios of activating to inhibitory natural killer cell receptors. These results support a contribution of innate responses to resistance against HIV‐1 infection. Scientific and ethical issues encountered during research in exposed uninfected subjects must be considered.     

Hepatitis C and HIV co—infection：a review

Co-infection with hepatitis C virus and human immunodeficiency virus is common in certain populations. Among HCV (+) persons, 10 % are also HIV (+), and among HIV (+) persons, 25 % are also HCV (+). Many studies have shown that in intravenous drug users, co-infection prevalence can be as high as 90-95 %. There is increasing evidence supporting the concept that people infected with HIV have a much more rapid course of their hepatitis C infection. Treatment of co-infection is often challenging because highly active anti-retroviral therapy (HAART) therapy is frequently hepatotoxic, especially in the presence of HCV. The purpose of this review is to describe the effects that HIV has on hepatitis C, the effects that hepatitis C has on HIV, and the treatment options in this challenging population.     

Why does HIV infection not lead to disseminated strongyloidiasis?

We investigated the hypothesis that host immunosuppression due to advancing human immunodeficiency virus (HIV) disease favors the direct development of infective larvae of Strongyloides stercoralis, which may facilitate hyperinfection and, hence, disseminated strongyloidiasis. To do this, we sought correlations between the immune status of the subjects and the development of S. stercoralis infections. Among 35 adults, there were significant negative rank correlations between CD4+ cell counts and the proportions of free-living male and female worms. Thus, in individuals with preserved immune function, direct development of S. stercoralis is favored, whereas, in individuals with lesser immune function, indirect development is relatively more common. These results may explain the notable absence of disseminated strongyloidiasis in advanced HIV disease. Because disseminated infection requires the direct development of infective larvae in the gut, the observed favoring of indirect development in individuals immunosuppressed by advancing HIV disease is not consistent with the promotion of disseminated infection.     

Coexistent sarcoidosis and HIV infection: an immunological paradox?

The CD4 lymphocyte plays a pivotal role in both sarcoidosis and HIV infection. Caring for a patient with both conditions represents a diagnostic and therapeutic challenge. We describe a patient, previously diagnosed with sarcoidosis, who subsequently contracted HIV infection. Manifestations of sarcoidosis were clinically silent until highly active anti-retroviral therapy was instituted. Her condition improved with the institution of corticosteroids. The diagnostic and therapeutic dilemmas encountered in patients with both conditions will be discussed including a complete review of the literature.     

Intestinal Kaposi''''s sarcoma may mimic gastrointestinal stromal tumor in HIV infection

Diffuse intestinal Kaposi's sarcoma shares macroscopicand histopathologic features with gastrointestinal stromatumors. Correct diagnosis may pose a clinical challengeWe describe the case of a young HIV-1-infected Africanlady without advanced immunodeficiency, who presentedwith a diffuse spindle cell tumor of the gut. Initiadiagnosis was of a gastrointestinal stromal tumor, basedon endoscopy and histopathology. Further evaluationrevealed evidence for human herpesvirus 8 (HHV8) andthe diagnosis had to be changed to diffuse intestinaKaposi's sarcoma. Antiretroviral triple therapy togethewith chemotherapy was commenced, and has led to therapid remission of intestinal lesions. With a backgroundof HIV infection, the presence of HHV8 as the causativeagent of Kaposi's sarcoma should be determined, asdistinct treatment is indicated.