scholarly journals Human Immunodeficiency Virus in the Brain—Culprit or Facilitator?

2018 ◽  
Vol 11 ◽  
pp. 117863371775268 ◽  
Author(s):  
Luminita Ene

Introduction: Human immunodeficiency virus (HIV) enters the brain early, where it can persist, evolve, and become compartmentalized. Central nervous system (CNS) disease can be attributed to HIV alone or to the complex interplay between the virus and other neurotropic pathogens. Aim: The current review aims to describe the direct impact of HIV on the brain as well as its relationship with other pathogens from a practitioner’s perspective, to provide a general clinical overview, brief workup, and, whenever possible, treatment guidance. Methods: A review of PubMed was conducted to identify studies on neuropathogenesis of HIV in relation to host responses. Furthermore, the interaction between the CNS pathogens and the host damage responses were revised in the setting of advanced and also well-controlled HIV infection. Results: Similar to other pathogens, HIV leads to CNS immune activation, inflammation, and viral persistence. Therefore, almost half of the infected individuals present with neurocognitive disorders, albeit mild. Compartmentalized HIV in the CNS can be responsible in a minority of cases for the dramatic presentation of symptomatic HIV escape. Disruption of the immune system secondary to HIV may reactivate latent infections or allow new pathogens to enter the CNS. Opportunistic infections with an inflammatory component are associated with elevated HIV loads in the cerebrospinal fluid and also with greater cognitive impairment. The inflammatory immune reconstitution syndrome associated with CNS opportunistic infections can be a life-threatening condition, which needs to be recognized and managed by efficiently controlling the pathogen burden and timely balanced combination antiretroviral therapy. Latent neurotropic pathogens can reactivate in the brain and mimic HIV-associated severe neurological diseases or contribute to neurocognitive impairment in the setting of stable HIV infection. Conclusions: As HIV can be responsible for considerable brain damage directly or by facilitating other pathogens, more effort is needed to recognize and manage HIV-associated CNS disorders and to eventually target HIV eradication from the brain.

2005 ◽  
Vol 12 (3) ◽  
pp. 168-177
Author(s):  
KL Mok ◽  
PG Kan

Human immunodeficiency virus (HIV) causes breakdown of the immune system and predisposes patients to various opportunistic infections and neoplasms. However, many patients may not be aware of the HIV infection before the development of their first HIV related complications. We reported four unrecognised HIV patients presenting to our accident and emergency department with common complications of HIV infection and the acquired immunodeficiency syndrome (AIDS). Although not as common as in America, emergency physicians in Hong Kong still have to take care of patients with unknown HIV status. The common presentations of HIV patients will be discussed. A high index of suspicion and knowledge of common HIV/AIDS complications are required for managing these patients.


Introduction, nutritional goals, and assessment 664 Unintentional weight and lean tissue loss 666 Cardiovascular risk and complications associated with HIV disease and treatment 667 Additional dietary issues 668 Untreated human immunodeficiency virus (HIV) infection leads to progressive suppression of immune function, eventually rendering the body susceptible to opportunistic infections and tumours. While there is no cure, antiretroviral therapy (ART) is highly effective in suppressing HIV replication. HIV disease is now a chronic condition and causes of death in this population have shifted from traditional AIDS-related illnesses to non-AIDS (Acquired Immune Deficiency Syndrome) events, the most common being atherosclerotic cardiovascular disease, liver disease, end-stage renal disease and non-AIDS–defining malignancies. There are a diverse range of nutritional conditions associated with HIV, reflecting the complexity of the disease and pharmacological management....


Author(s):  
Avindra Nath

It has been nearly three decades since the first descriptions of the neurological comploications of HIV infection. During this period of time there has been tremendous progress in defining the clinical syndromes, modes of diagnosis, detailed pathophysiology and modes of treatment. Many of the dreaded complications are now manageable particularly if diagnosed early. However, neurocognitive impairment associated with HIV infection still remains a significant cause of morbidity and much is needed to control; the effects of the virus on the brain and for the eventual eradication of the virus from the brain reservoir.


Author(s):  
Eihab Subahi ◽  
safwan aljafar ◽  
haidar barjas ◽  
Mohamed Abdelrazek ◽  
Fatima Rasoul

Opportunistic infections are common in human immunodeficiency virus (HIV)-infected patients. Co-infections with Cryptococcus neoformans together with Mycobacterium and Pneumocystis jiroveci pneumonia (PCP) are rare, and typically occur in immunocompromised individuals, particularly AIDS patients.


2019 ◽  
Vol 144 (5) ◽  
pp. 572-579 ◽  
Author(s):  
Sobia Nizami ◽  
Cameron Morales ◽  
Kelly Hu ◽  
Robert Holzman ◽  
Amy Rapkiewicz

Context.— With increasing use and efficacy of antiretroviral therapy for human immunodeficiency virus (HIV) infection, deaths from acquired immunodeficiency syndrome (AIDS)–defining conditions have decreased. Objective.— To examine trends in the cause of death of HIV-infected patients who underwent autopsy at a major New York City hospital from 1984 to 2016, a period including the major epochs of the AIDS epidemic. Design.— Retrospective review of autopsy records and charts with modeling of trends by logistic regression using polynomial models. Results.— We identified 252 autopsies in adult patients with AIDS (by 1982 definition) or HIV infection. Prior to widespread use of highly active antiretroviral therapy, in 1984–1995, on average 13 autopsies per year were done. Post–highly active antiretroviral therapy, the average number of autopsies declined to 4.5 per year. The fitted mean age at death was 35 years in 1984 and increased curvilinearly to 46 years (95% CI, 43–49) in 2016 (P < .001). By regression analysis, mean CD4+ T-cell count increased from 6 in 1992 to 64 in 2016 (P = .01). The proportion of AIDS-defining opportunistic infections decreased, from 79% in 1984–1987 to 41% in 2008–2011 and 29% in 2012–2016 (P = .04). The frequency of nonopportunistic infections, however, increased from 37% in 1984–1987 to 73% in 2008–2011 and 57% in 2012–2016 (P = .001). The frequency of AIDS-defining and other malignancies did not change significantly during the study period. The prevalence of atherosclerosis at autopsy rose dramatically, from 21% in 1988–1991 to 54% in 2008–2011 (P < .001). Conclusions.— Despite limitations of autopsy studies, many trends in the evolution of the HIV/AIDS epidemic are readily discernable.


1994 ◽  
Vol 7 (1) ◽  
pp. 14-28 ◽  
Author(s):  
C M Tsoukas ◽  
N F Bernard

Human immunodeficiency virus (HIV) interacts with the immune system throughout the course of infection. For most of the disease process, HIV activates the immune system, and the degree of activation can be assessed by measuring serum levels of molecules such as beta 2-microglobulin and neopterin, as well as other serum and cell surface phenotype markers. The levels of some of these markers correlate with clinical progression of HIV disease, and these markers may be useful as surrogate markers for development of clinical AIDS. Because the likelihood and timing of development of clinical AIDS following seroconversion, for any particular individual, are not readily predictable, the use of nonclinical disease markers has become critically important to patient management. Surrogate markers of HIV infection are, by definition, measurable traits that correlate with disease progression. An ideal marker should identify patients at highest risk of disease progression, provide information on how long an individual has been infected, help in staging HIV disease, predict development of opportunistic infections associated with AIDS, monitor the therapeutic efficacy of immunomodulating or antiviral treatments, and the easily quantifiable, reliable, clinically available, and affordable. This review examines the current state of knowledge and the role of surrogate markers in the natural history and treatment of HIV infection. The clinical usefulness of each marker is assessed with respect to the criteria outlined for the ideal surrogate marker for HIV disease progression.


2019 ◽  
Vol 6 (03) ◽  
pp. 4384-4389
Author(s):  
Ajay Nathan ◽  
KS Brar ◽  
Arun K Valsan ◽  
Nimitha K Mohan ◽  
Gautam Singh

Aim: To find Prevalence, Aetiology and Clinical Spectrum of abnormal adrenal functions in Human Immunodeficiency Virus infection. To diagnose and treat adrenal dysfunction in various stages of HIV infection and see the response to treatment if required. Material & Methods: 100 patients with HIV infection being admitted to our hospital was evaluated for abnormal adreno cortical functions. Immune dysfunction was assessed with CD4 count. Statistical tests (chi squared test) were applied to the collected data to find out any significant correlations. Results: The overall prevalence of adrenocortical abnormalities in HIV positive patients was 14% which included hypocortisolemia in 3% and hypercortisolemia in 11% of patients. Frequency of hypocortisolemia was significantly associated with presence of HIV infection with opportunistic infections and low CD4 counts (less than 50cells). In patients having hypercortisolemia, ONDST (Over night dexamethasone suppression test) was done and it showed reduction of serum cortisol to expected level (suppressed to <1.8 mcg/dl). Adjustment disorders and drugs mainly efavirnz more than nevirapine was incriminated in the same. Conclusion: HPA axis dysfunction is frequently encountered in HIV infected patients. The commonest dysfunction was hypercortisolemia probably due to elevated cytokines. Hypercortisolemia is a feature of early stage HIV infection. The likelihood of adrenal insufficiency increases as the disease advances and patient enters a more immunocompromised state. Hypocortisolemia should be treated regardless of the existence of associated symptoms. Hypercortisolemia in the absence of features of Cushing’s syndrome is common and should not promote treatment or specific studies.


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