Vasculitis during human acquired immunodeficiency virus infection

Vasculitis is among the dysimmunity-mediated disorders seen in patients infected with the human immunodeficiency virus (HIV). Several cases have been reported. The central and peripheral nervous systems were the main targets, although many other organs may be involved. There were wide variations in clinical presentation, clinico-pathologic patterns, and the stage of the HIV infection at vasculitis onset. Causes included drugs and infections, particularly some opportunistic infections. In some cases, the vasculitis seemed to be directly due to the HIV. The etiopathogenesis remains unclear and the treatment unstandardized. Four cases of systemic vasculitis in HIV-infected patients are reported herein. All four patients received the treatment recommended for hepatitis B virus-related polyarteritis nodosa, namely plasma exchange and antiretroviral drugs.     

Prevalence of central nervous system cryptococcosis in human immunodeficiency virus reactive hospitalized patients

Central nervous system cryptococcosis is an important cause of mortality among human immunodeficiency virus (HIV) reactive patients. A retrospective study was conducted on a total of 1,863 HIV reactive hospitalized patients suspected of cryptococcal meningitis. Three hundred and fifty-nine cerebrospinal fluid specimens of these cases were screened for various cryptococcal investigations. Thirty-nine out of 359 (10.86%) showed a definite diagnosis of cryptococcosis with a mortality rate of 25.64%. Prevalence of cryptococcal meningitis in the total HIV reactive cohort was 2.09%. Concurrent cryptococcal meningitis and tuberculosis was seen in 33.3% cases. A high index of clinical suspicion and routine mycological surveillance is required to help an early diagnosis and appropriate therapy, as majority of patients respond well to therapy if treated early.     

人胸腺组织原代培养细胞与人类免疫缺陷病毒间的相互作用

背景：人类免疫缺陷病毒能够结合人胸腺的细胞CD4受体,从而导致CD4细胞活性降低。 目的：观察人胚胎胸腺组织原代培养与人类免疫缺陷病毒相互作用关系。 方法：取人胎胸腺组织进行原代细胞培养,取胸腺的细胞与人类免疫缺陷病毒1 ⅢB混合培养设为实验组,设置不加人类免疫缺陷病毒培养的胸腺的细胞为对照组。 结果与结论：透射电镜观察显示,培养40 h,人类免疫缺陷病毒诱导的胸腺的细胞内即可发现大量艾滋病病毒颗粒。MTT法和免疫组织化学染色检测结果显示,培养40 h~22 d,HIV诱导胸腺的细胞吸光度值均显著低于对照组(r=0.9733,P < 0.05),人类免疫缺陷病毒诱导胸腺的细胞膜上和细胞浆Fas-L阳性表达率均升高(P < 0.05)。说明人类免疫缺陷病毒可致原代培养的人胚胎胸腺的细胞活性降低。     

Meningitis caused by Rhodotorula rubra in an human immunodeficiency virus infected patient

Rhodotorula spp. are common saprophytes but may be responsible for systemic infections in immunocompromised patients. Meningitis caused by Rhodotorula spp. in human immunodeficiency virus (HIV) infected patients has been reported only rarely. We present a case of meningitis caused by Rhodotorula rubra in HIV infected patient. The presumptive diagnosis of cryptococcal meningitis was made on the basis of India ink preparation, Gram staining and latex agglutination test (LAT) for cryptococcal antigen. The final diagnosis was confirmed by isolation of Rhodotorula rubra from cerebrospinal fluid on culture. LAT was considered false positive. Amphotericin B and 5-fluorocytosine were administered but the patient succumbed to his illness.     

Human immunodeficiency virus type 1 reference materials

Since licensure of the first human immunodeficiency virus type 1 screening assay in March 1985, there has been a need for well-characterized human immunodeficiency virus type 1 reference sera. These sera would be used in an effort to ensure uniformity of human immunodeficiency virus type 1 test results worldwide. Three major organizations--the World Health Organization, the Pan American Health Organization, and the National Committee for Clinical Laboratory Standards working with the College of American Pathologists--have ongoing programs aimed at the preparation of these reference sera. All three organizations are preparing both negative and human immunodeficiency virus type 1 seropositive sera. In addition, one organization is preparing early sero-converter and late acquired immunodeficiency syndrome samples. The status of these efforts and the serologic characteristics of the sera were reviewed.     

Cellular latency of human immunodeficiency virus type 1.

The infection of humans by human immunodeficiency virus type 1 is characterized by a prolonged stage of clinical quiescence. This clinically asymptomatic period may be based, in part, on the development of cell populations within the body that maintain human immunodeficiency virus type 1 in a state of latency. Recent advances in the understanding of the molecular mechanisms involved in various forms of cellular latency of human immunodeficiency virus type 1 have begun to shed light on the variable period of asymptomatic infection. The elucidation of cellular retroviral latency, in vivo, will also be critical to the design of novel therapeutic approaches with which to combat human immunodeficiency virus type 1 infections.     

Isolation of HTLV-III from cerebrospinal fluid and neural tissues of patients with neurologic syndromes related to the acquired immunodeficiency syndrome

We conducted virus-isolation studies on 56 specimens from the nervous system of 45 patients in order to determine whether human T-cell lymphotropic virus Type III (HTLV-III) is directly involved in the pathogenesis of the neurologic disorders frequently encountered in the acquired immunodeficiency syndrome (AIDS) and the AIDS-related complex. We recovered HTLV-III from at least one specimen from 24 of 33 patients with AIDS-related neurologic syndromes. In one patient, HTLV-III was isolated from the cerebrospinal fluid during acute aseptic meningitis associated with HTLV-III seroconversion. HTLV-III was also isolated from cerebrospinal fluid from six of seven patients with AIDS or its related complex and unexplained chronic meningitis. In addition, of 16 patients with AIDS-related dementia, 10 had positive cultures for HTLV-III in cerebrospinal fluid, brain tissue, or both. Furthermore, we cultured HTLV-III from the spinal cord of a patient with myelopathy and from the sural nerve of a patient with peripheral neuropathy. These findings suggest that HTLV-III is neurotropic, is capable of causing acute meningitis, is responsible for AIDS-related chronic meningitis and dementia, and may be the cause of the spinal-cord degeneration and peripheral neuropathy in AIDS and AIDS-related complex.     

Cryptococcal meningitis caused by Cryptococcus neoformans var. gattii, serotype C, in AIDS patients in Soweto, South Africa.

We present four patients from South Africa with meningitis caused by Cryptococcus neoformans var. gattii, serotype C. These are the first patients with human immunodeficiency virus (HIV) infection to be reported with serotype C meningitis.     

Detection of human immunodeficiency viruses by the polymerase chain reaction

The human immunodeficiency viruses types 1 and 2 have been implicated as the etiologic agent of the acquired immunodeficiency syndrome and its related disorders. The direct detection of human immunodeficiency virus is complicated by the low incidence of free circulating virus as well as the small number of infected cells. An in vitro DNA amplification procedure known as the polymerase chain reaction has been applied to the detection of the human immunodeficiency virus proviral sequences in infected individuals. This article highlights the features of the polymerase chain reaction and its contribution to the detection of these viruses.     

Biopsy diagnosis in human immunodeficiency virus infection and acquired immunodeficiency syndrome

Human immunodeficiency virus infection and the complications of the acquired immunodeficiency syndrome produce a broad spectrum of lesions affecting all organs and tissues. They are caused by uncommon etiologic agents and characterized by unusual location, multiplicity, rapid progression, and tendency to generalization. Cellular reactions are inefficient and histologic appearances frequently atypical. Tissue biopsy, most often endoscopic, with microscopic examination, is the method predominantly used for achieving the required rapid, definitive diagnosis. This article reviews the lesions commonly seen in biopsy specimens of human immunodeficiency virus infection and acquired immunodeficiency disease syndrome, their characteristic histologic features, and their differential diagnosis.     

Neuronal injury in hippocampus with human immunodeficiency virus transactivating protein,Tat

Patients with human immunodeficiency virus infection may develop a dementing illness. Using both in vitro and in vivo models, we investigated the susceptibility of the hippocampal formation to the Tat protein of human immunodeficiency virus. We also determined the pattern of hippocampal injury in patients with human immunodeficiency virus encephalitis. Following exposure of hippocampal slices to Tat, marked susceptibility of CA3 region with relative insensitivity of the CA1/2 region was observed. Injection of Tat into different regions of the rat hippocampus produced similar neuronal loss in both CA3 region and the dentate gyrus. In animals administered Tat, lesions were dose-dependent and immunohistochemical staining showed marked gliosis and loss of microtubule associated protein-2 in the affected areas at 3 days post-injection. Interestingly, synaptophysin staining was relatively preserved. In hippocampal tissue from patients with human immunodeficiency virus encephalitis, loss of microtubule-associated protein-2 staining was reduced in the molecular layer of the dentate gyrus.The results of our experiments demonstrate a unique pattern of hippocampal injury in organotypic culture and rats exposed to Tat. Our observations that patients with human immunodeficiency virus reveal a similar pattern of damage suggests that Tat protein may be pathophysiological relevant in human immunodeficiency virus encephalitis.     

Progressive multifocal leukoencephalopathy and retroviral encephalitis in acquired immunodeficiency syndrome

Antigens of human polyomaviruses, the etiologic agents of progressive multifocal leukoencephalopathy (PML), and of human immunodeficiency virus were localized in paraffin sections from brains of six patients who died with the acquired immunodeficiency syndrome. Immunostaining revealed polyomaviral antigens in oligodendrocytes and in some astrocytes. Human immunodeficiency (retro) virus antigens were immunostained in mononuclear macrophages, glial cells, and vascular endothelial cells. Both viral types were found ultrastructurally. The lesions of PML were more destructive than is usually seen in cases without the acquired immunodeficiency syndrome. The retroviral encephalitis could have occurred before the onset of PML. However, a secondary retroviral encephalitis could have resulted if the monocytes responding to an initial polyomaviral lesion were already infected with human immunodeficiency virus before they differentiated into macrophages.     

Elevated levels of CD4 antigen in sera of human immunodeficiency virus-infected populations.

CD4 antigen levels in sera from asymptomatic intravenous drug users and homosexuals and patients with lymphadenopathy, acquired immunodeficiency syndrome-related complex, or acquired immunodeficiency syndrome were quantitated. Like soluble CD8, CD4 antigen levels were elevated in human immunodeficiency virus-seronegative asymptomatic intravenous drug users and homosexuals, probably reflecting infections such as cytomegalovirus, Epstein-Barr virus, and hepatitis B virus infections. The sera from human immunodeficiency virus-seropositive groups of patients with human immunodeficiency virus infection also had elevated levels of CD4 antigen, presumably reflecting infections like cytomegalovirus and human immunodeficiency virus infections.     

Meningitis and endocarditis caused by group B streptococcus in a human immunodeficiency virus (HIV) infected patient

We present a case of meningitis and endocarditis caused by Streptococcus agalactiae (group B streptococcus) in an adult patient with human immunodeficiency virus (HIV) infection. To our knowledge, only four other cases of meningitis, none of which had concomitant endocarditis, have been reported so far. A 45-year-old homosexual patient presented with fever, confusion, and signs of meningeal irritation. Streptococcus agalactiae was cultured from the blood, urine, and cerebrospinal fluid (CSF). Diagnosis of meningitis caused by streptococcus agalactiae was made. On day 35, a heart murmur was noticed, and patient developed cardiac decompensation. Echocardiography revealed vegetations on the mitral and aortic valve. After nine weeks of antibiotic treatment, the patient was discharged from the hospital in good general condition, with improved CSF and echocardiographic findings.     

How human immunodeficiency virus ravages the immune system.

The immune system of individuals infected with human immunodeficiency virus is affected in two distinct ways: by loss of CD4+ cells and by loss of T-helper-cell function. Neither of these processes is yet fully understood. Research during 1991 that investigated the interaction between human immunodeficiency virus and the immune system has raised as many questions as it answered. Nevertheless, many of the issues raised are relevant to mechanisms responsible for the ravaging of the immune system by human immunodeficiency virus.     

Photodynamic inactivation of simian immunodeficiency virus

A photodynamic flow system employing a dihematoporphyrin ether (DHE) was tested for its ability to inactivate the in vitro infectivity of simian immunodeficiency virus (SICMac) at 630 +/- 5 nm with a light fluence of 5 J/cm2. Cell-free SIVMac was inactivated by photoactivated hematoporphyrin derivative in a dose-dependent fashion. Since SIVMac is closely related to human immunodeficiency virus type 2 (HIV-2) and we have previously reported the successful photodynamic inactivation of HIV-1 in cell-free medium as well as in whole human blood, this technology has the potential for the eradication of transfusion-associated acquired immunodeficiency diseases caused by the above-mentioned retroviruses.     

Dermatopathological challenges in the human immunodeficiency virus and acquired immunodeficiency syndrome era

Ramdial P K
(2010) Histopathology 56 , 39–56
Dermatopathological challenges in the human immunodeficiency virus and acquired immunodeficiency syndrome era The histopathological assessment of cutaneous lesions is critical to the definitive diagnosis of many human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome‐associated dermatoses, infections and tumours. Dermatopathological challenges stem mainly from the altered histopathological profile of established cutaneous entities compared with that in the HIV‐unaffected population, the emergence of new diseases and the impact of therapeutic modalities on cutaneous lesions. This review focuses on some of these diagnostic dilemmas, with emphasis on the following challenges: (i) infective diagnostic pitfalls; (ii) itchy papular skin lesions; (iii) co‐lesional comorbid diseases; (iv) drug‐induced disease alterations; and (v) neoplastic and pseudoneoplastic proliferations. The drug‐induced alterations include highly active antiretroviral therapy‐associated disease modifications.