HIV AIDS natural history, complications, and prognosis: Difference between revisions

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Latest revision as of 22:30, 20 September 2021

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2] ; Alejandro Lemor, M.D. [3]

Overview

There is currently no cure for HIV/AIDS. HIV infection leads to progressive decline in CD4+ T-lymphocyte count increasing the risk for opportunistic infections and malignancies. Despite having a variable rate of progression determined by specific host and viral factors, the median time from infection to the development of AIDS ranges from 8 to 10 years among untreated individuals.^[1] With the advent of highly active antiretroviral therapy (HAART), both morbidity and mortality have dramatically decreased. Survival and the rate of CD4-count recovery is influenced by age, baseline CD4 cell count, baseline viral load and initial and sustained viral suppression.^[2] In areas where HAART is widely available, the development of HAART as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly-diagnosed HIV-infected person to near normal (assuming full compliance to HAART).^[3] HIV infection makes individuals highly susceptible to severe opportunistic infections and neoplastic disease. Major complications of HIV/AIDS include Pneumocystis jirovecii pneumonia, disseminated Mycobacterium avium complex infection, cryptococcal meningitis, cytomegalovirus retinitis, Kaposi sarcoma, and primary CNS lymphoma.

Natural History

In the early days of the HIV epidemic, knowledge about the natural history of HIV accrued rapidly. However, the widespread use of effective antiretroviral therapy (ART) brought a shift in focus of the research community away from studies of natural history to those of treated infection.^[4] HIV infection leads to progressive decline in CD4+ T-lymphocyte count increasing the risk for opportunistic infections and malignancies. Despite having a variable rate of progression determined by specific host and viral factors, the median time from infection to the development of AIDS ranges from 8 to 10 years among untreated individuals.^[1] With the advent of highly active antiretroviral therapy (HAART), both morbidity and mortality have dramatically decreased. Survival and the rate of CD4-count recovery is influenced by age, baseline CD4 cell count, baseline viral load and initial and sustained viral suppression.^[2]

Disease Progression

Natural history of untreated HIV - By Sigve - Own work, CC0, https://commons.wikimedia.org/w/index.php?curid=15383502

Acute HIV syndrome

Approximately half of patients that acquire HIV develop a mononucleosis-like syndrome within 3-6 weeks during which the viral titers are very elevated. Common symptoms include acute but brief and nonspecific influenza-like retroviral syndrome that can include fever, malaise, lymphadenopathy, pharyngitis, arthritis, or skin rash.^[5] This causes a rapid drop in CD4 T-Cell count as these cells are the primary host for viral replication. Within several weeks patients mount a strong immune response to the virus that causes a drop in the viral titers. However, this response is not adequate to completely suppress viral replication. Although viremia may become undetectable, replication persists in the lymphoid organs. Although a significant number of patients do not have an acute HIV syndrome, these processes do occur albeit without symptoms.^[6]

Clinical Latency

This period is sometimes called asymptomatic HIV infection or chronic HIV infection. After the initial phase, the majority of patients with HIV develop a clinical latency period that lasts several years. During this period, all patients have a progressive decline in immune status and gradual depletion of CD4 T-cells. This period does not represent a true microbiological or pathological latency, but rather defines a time period without clinically manifest disease. People who are on highly active antiretroviral therapy (HAART) may live with clinical latency for several decades.^[6]

Clinically Apparent Disease (AIDS)

The eventual outcome of most HIV infections is gradual immune system deterioration resulting in AIDS. Clinically apparent disease is classically diagnosed following an AIDS-defining illness i.e. an opportunistic infection or neoplasm that demonstrates a significant compromise of the immune system. Another diagnostic sign, although not strictly clinical, is the decline of CD4 T-cell count below 200 cells/mm³. Without treatment, individuals diagnosed with AIDS may survive approximately 1-3 years.^[6]

Distinct Patterns of Progression

The natural course of untreated HIV infection varies widely. The past decade has seen considerable interest in the identification of subgroups of HIV-positive persons who exhibit distinct patterns of disease progression:^[4]

Long-term nonprogressors (LTNP) are individuals who remain asymptomatic for a prolonged period of time off ART with a high CD4 cell count. Although it is widely reported that 1–5% of the HIV-positive population are LTNP, these estimates are complicated by the fact that there is no standardized definition of a LTNP, and thus definitions used (and the way in which they are applied, particularly in the presence of varying follow-up and irregularly measured CD4 cell counts) differ widely. LTNP status can be lost, and thus the reported prevalence of LTNP within a study will depend on the required period of follow-up. Predictors of loss of LTNP status are a high baseline HIV DNA level and a more rapid increase in HIV DNA over the first year of follow-up, suggesting the presence of ongoing (but low-grade) viral replication. Indeed, HIV RNA levels in plasma increased by 0.04 log10 copies/ml per year over the first 8 years after diagnosis. As such, it is likely that virtually all HIV-positive persons will eventually experience disease progression if left untreated.^[4]

Elite controllers or viral controllers are individuals who are able to suppress HIV replication to such an extent that viral load levels remain undetectable in the absence of ART. As with LTNP, several studies have attempted to identify factors associated with elite controller status. Loss of naive CD4 T cells seems to be a universal feature of elite controllers, despite the ability of such individuals to maintain undetectable viral loads. However, CD4 naive lymphocytes from elite controllers tend to be less susceptible to HIV infection than such lymphocytes from progressors or uninfected individuals. This specific feature was linked with upregulation of a cellular kinase (p21). HIV-specific CD4 activation is a hallmark of viral control but, many other host factors have been linked with this phenotype, including cellular restriction factors such as APOBEC, tetherin, and SAMHD1. In addition, several viral factors may also play a role, including deletions or mutations with the viral genes that may have an impact on the ability of the virus to replicate. ^[4]

Complications

HIV infection makes individuals highly susceptible to severe opportunistic infections and neoplastic disease. The following complications are classically observed among patients with significant immunocompromise and rarely manifest among patients with a CD4 count greater than 350 cells/mm³.

Prognosis

Without treatment, the net median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype, and the median survival rate after diagnosis of AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months, depending on the study.^[7] In areas where it is widely available, the development of HAART as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly-diagnosed HIV-infected person to near normal (assuming full compliance to HAART).^[8]

References

↑ ^1.0 ^1.1 Vergis EN, Mellors JW (2000). "Natural history of HIV-1 infection". Infect Dis Clin North Am. 14 (4): 809–25, v–vi. PMID 11144640.
↑ ^2.0 ^2.1 Giles M, Workman C (2009). "Clinical manifestations and the natural history of HIV" (PDF). Australian Society for HIV Management: 125–32. ISBN 9781920773571.
↑ Knoll B, Lassmann B, Temesgen Z (2007). "Current status of HIV infection: a review for non-HIV-treating physicians". Int J Dermatol. 46 (12): 1219–28. doi:10.1111/j.1365-4632.2007.03520.x. PMID 18173512.
↑ ^4.0 ^4.1 ^4.2 ^4.3 Sabin CA, Lundgren JD (2013). "The natural history of HIV infection". Curr Opin HIV AIDS. 8 (4): 311–7. doi:10.1097/COH.0b013e328361fa66. PMC 4196796. PMID 23698562.CS1 maint: PMC format (link)
↑ Workowski KA, Bachmann LH, Chan PA, Johnston CM, Muzny CA, Park I; et al. (2021). "Sexually Transmitted Infections Treatment Guidelines, 2021". MMWR Recomm Rep. 70 (4): 1–187. doi:10.15585/mmwr.rr7004a1. PMC 8344968 Check |pmc= value (help). PMID 34292926 Check |pmid= value (help).
↑ ^6.0 ^6.1 ^6.2 Pantaleo G, Graziosi C, Fauci AS (1993). "New concepts in the immunopathogenesis of human immunodeficiency virus infection". N Engl J Med. 328 (5): 327–35. doi:10.1056/NEJM199302043280508. PMID 8093551.
↑ Template:Cite paper
↑ Knoll B, Lassmann B, Temesgen Z (2007). "Current status of HIV infection: a review for non-HIV-treating physicians". Int J Dermatol. 46 (12): 1219–28. doi:10.1111/j.1365-4632.2007.03520.x. PMID 18173512.

Template:WH Template:WS

[pmid11144640-1] 1.0 ^1.1 Vergis EN, Mellors JW (2000). "Natural history of HIV-1 infection". Infect Dis Clin North Am. 14 (4): 809–25, v–vi. PMID 11144640.

[aust-2] 2.0 ^2.1 Giles M, Workman C (2009). "Clinical manifestations and the natural history of HIV" (PDF). Australian Society for HIV Management: 125–32. ISBN 9781920773571.

[3] Knoll B, Lassmann B, Temesgen Z (2007). "Current status of HIV infection: a review for non-HIV-treating physicians". Int J Dermatol. 46 (12): 1219–28. doi:10.1111/j.1365-4632.2007.03520.x. PMID 18173512.

[pmid23698562-4] 4.0 ^4.1 ^4.2 ^4.3 Sabin CA, Lundgren JD (2013). "The natural history of HIV infection". Curr Opin HIV AIDS. 8 (4): 311–7. doi:10.1097/COH.0b013e328361fa66. PMC 4196796. PMID 23698562.CS1 maint: PMC format (link)

[pmid34292926-5] Workowski KA, Bachmann LH, Chan PA, Johnston CM, Muzny CA, Park I; et al. (2021). "Sexually Transmitted Infections Treatment Guidelines, 2021". MMWR Recomm Rep. 70 (4): 1–187. doi:10.15585/mmwr.rr7004a1. PMC 8344968 Check |pmc= value (help). PMID 34292926 Check |pmid= value (help).

[pmid8093551-6] 6.0 ^6.1 ^6.2 Pantaleo G, Graziosi C, Fauci AS (1993). "New concepts in the immunopathogenesis of human immunodeficiency virus infection". N Engl J Med. 328 (5): 327–35. doi:10.1056/NEJM199302043280508. PMID 8093551.

[7] Template:Cite paper

[8] Knoll B, Lassmann B, Temesgen Z (2007). "Current status of HIV infection: a review for non-HIV-treating physicians". Int J Dermatol. 46 (12): 1219–28. doi:10.1111/j.1365-4632.2007.03520.x. PMID 18173512.

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@@ Line 2: / Line 2: @@
 {{AIDS}}
-{{CMG}} ; {{Ammu}} ; {{AL}}
+{{CMG}}; {{AE}} {{Ammu}} ; {{AL}}
 ==Overview==
-Currently there is no cure for [[AIDS]] but taking treatment dramatically increased the amount of time people with [[HIV]] remain alive. Research continues in the areas of drug treatments and [[vaccine]] development. Unfortunately, [[HIV medications]] are not always available in the developing world, where the bulk of cases now occur.
+There is currently no cure for HIV/[[AIDS]].  HIV infection leads to progressive decline in CD4+ T-lymphocyte count increasing the risk for opportunistic infections and malignancies. Despite having a variable rate of progression determined by specific host and viral factors, the median time from infection to the development of AIDS ranges from 8 to 10 years among untreated individuals.<ref name="pmid11144640">{{cite journal| author=Vergis EN, Mellors JW| title=Natural history of HIV-1 infection. | journal=Infect Dis Clin North Am | year= 2000 | volume= 14 | issue= 4 | pages= 809-25, v-vi | pmid=11144640 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11144640  }} </ref> With the advent of highly active antiretroviral therapy (HAART), both morbidity and mortality have dramatically decreased. Survival and the rate of CD4-count recovery is influenced by age, baseline CD4 cell count, baseline viral load and initial and sustained viral suppression.<ref name="aust">{{cite journal| author=Giles M, Workman C| title=Clinical manifestations and the natural history of HIV | journal=Australian Society for HIV Management | year= 2009 | pages= 125-32 | isbn=9781920773571 | url=http://www.ashm.org.au/images/Publications/Monographs/HIV_Management_Australasia/HIV-Management-Australia-2009.pdf  }} </ref>  In areas where HAART is widely available, the development of [[HAART]] as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly-diagnosed HIV-infected person to near normal (assuming full compliance to HAART).<ref>{{cite journal |journal= Int J Dermatol |date=2007 |volume=46 |issue=12 |pages=1219–28 |title= Current status of HIV infection: a review for non-HIV-treating physicians |author= Knoll B, Lassmann B, Temesgen Z |pmid=18173512 |doi=10.1111/j.1365-4632.2007.03520.x |pmid=18173512}}</ref>  HIV infection makes individuals highly susceptible to severe opportunistic infections and neoplastic disease. Major complications of HIV/AIDS include ''[[Pneumocystis jirovecii]]'' pneumonia, disseminated [[Mycobacterium avium complex]] infection, [[Cryptococcus|cryptococcal meningitis]], [[cytomegalovirus]] retinitis, [[Kaposi sarcoma]], and [[primary CNS lymphoma]].
-[[Opportunistic infections]] and other coinfections that might be common in HIV-infected persons, such as [[sexually transmitted infections]], can also have adverse effects on the natural history of HIV infection.
 ==Natural History==
-In the early days of the HIV epidemic, knowledge about the natural history of HIV accrued rapidly. However, the widespread use of effective antiretroviral therapy (ART) brought a shift in focus of the research community away from studies of natural history to those of treated infection.<ref name="pmid23698562">{{cite journal| author=Sabin CA, Lundgren JD| title=The natural history of HIV infection. | journal=Curr Opin HIV AIDS | year= 2013 | volume= 8 | issue= 4 | pages= 311-7 | pmid=23698562 | doi=10.1097/COH.0b013e328361fa66 | pmc=PMC4196796 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23698562  }} </ref>  HIV infection leads to progressive decline in CD4+ T-lymphocyte count increasing the risk for opportunistic infections and malignancies. Despite having a variable rate of progression determined by specific host and viral factors, the median time from infection to the development of AIDS ranges from 8 to 10 years among untreated individuals.<ref name="pmid11144640">{{cite journal| author=Vergis EN, Mellors JW| title=Natural history of HIV-1 infection. | journal=Infect Dis Clin North Am | year= 2000 | volume= 14 | issue= 4 | pages= 809-25, v-vi | pmid=11144640 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11144640  }} </ref> With the advent of highly active antiretroviral therapy (HAART), survival increases and CD4 cell recovery occurs at varying rates. The rate of recovery is influenced by age, baseline CD4 cell count, baseline viral load and initial and sustained viral suppression.<ref name="aust">{{cite journal| author=Giles M, Workman C| title=Clinical manifestations and the natural history of HIV | journal=Australian Society for HIV Management | year= 2009 | pages= 125-32 | isbn=9781920773571 | url=http://www.ashm.org.au/images/Publications/Monographs/HIV_Management_Australasia/HIV-Management-Australia-2009.pdf  }} </ref>
+In the early days of the HIV epidemic, knowledge about the natural history of HIV accrued rapidly. However, the widespread use of effective antiretroviral therapy (ART) brought a shift in focus of the research community away from studies of natural history to those of treated infection.<ref name="pmid23698562">{{cite journal| author=Sabin CA, Lundgren JD| title=The natural history of HIV infection. | journal=Curr Opin HIV AIDS | year= 2013 | volume= 8 | issue= 4 | pages= 311-7 | pmid=23698562 | doi=10.1097/COH.0b013e328361fa66 | pmc=PMC4196796 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23698562  }} </ref>  HIV infection leads to progressive decline in CD4+ T-lymphocyte count increasing the risk for opportunistic infections and malignancies. Despite having a variable rate of progression determined by specific host and viral factors, the median time from infection to the development of AIDS ranges from 8 to 10 years among untreated individuals.<ref name="pmid11144640">{{cite journal| author=Vergis EN, Mellors JW| title=Natural history of HIV-1 infection. | journal=Infect Dis Clin North Am | year= 2000 | volume= 14 | issue= 4 | pages= 809-25, v-vi | pmid=11144640 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11144640  }} </ref> With the advent of highly active antiretroviral therapy (HAART), both morbidity and mortality have dramatically decreased. Survival and the rate of CD4-count recovery is influenced by age, baseline CD4 cell count, baseline viral load and initial and sustained viral suppression.<ref name="aust">{{cite journal| author=Giles M, Workman C| title=Clinical manifestations and the natural history of HIV | journal=Australian Society for HIV Management | year= 2009 | pages= 125-32 | isbn=9781920773571 | url=http://www.ashm.org.au/images/Publications/Monographs/HIV_Management_Australasia/HIV-Management-Australia-2009.pdf  }} </ref>
 ===Disease Progression===
-[[File:HIV_natural_history.png|thumb|700px|center|Natural history of untreated HIV]]
+[[File:HIV_natural_history.png|thumb|700px|center|Natural history of untreated HIV - By Sigve - Own work, CC0, https://commons.wikimedia.org/w/index.php?curid=15383502]]
 ====Acute HIV syndrome====
-Approximately half of patients that acquire HIV develop a mononucleosis-like syndrome within 3-6 weeks during which the viral titers are very elevated. This causes a rapid drop in CD4 T-Cell count as these cells are the primary host for viral replication. Within several weeks patients mount a strong immune response to the virus that causes a drop in the viral titers. However, this response is not adequate to completely suppress viral replication. Although viremia may become undetectable, replication persists in the lymphoid organs. Although a significant number of patients do not have an acute HIV syndrome, these processes do occur albeit without symptoms.<ref name="pmid8093551">{{cite journal| author=Pantaleo G, Graziosi C, Fauci AS| title=New concepts in the immunopathogenesis of human immunodeficiency virus infection. | journal=N Engl J Med | year= 1993 | volume= 328 | issue= 5 | pages= 327-35 | pmid=8093551 | doi=10.1056/NEJM199302043280508 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8093551  }} </ref>
+Approximately half of patients that acquire HIV develop a mononucleosis-like syndrome within 3-6 weeks during which the viral titers are very elevated. Common symptoms include [[acute]] but brief and nonspecific [[influenza]]-like [[retroviral syndrome]] that can include [[fever]], [[malaise]], [[lymphadenopathy]], [[pharyngitis]], [[arthritis]], or [[skin rash]].<ref name="pmid34292926">{{cite journal| author=Workowski KA, Bachmann LH, Chan PA, Johnston CM, Muzny CA, Park I | display-authors=etal| title=Sexually Transmitted Infections Treatment Guidelines, 2021. | journal=MMWR Recomm Rep | year= 2021 | volume= 70 | issue= 4 | pages= 1-187 | pmid=34292926 | doi=10.15585/mmwr.rr7004a1 | pmc=8344968 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=34292926  }} </ref> This causes a rapid drop in CD4 T-Cell count as these cells are the primary host for viral replication. Within several weeks patients mount a strong immune response to the virus that causes a drop in the viral titers. However, this response is not adequate to completely suppress viral replication. Although viremia may become undetectable, replication persists in the lymphoid organs. Although a significant number of patients do not have an acute HIV syndrome, these processes do occur albeit without symptoms.<ref name="pmid8093551">{{cite journal| author=Pantaleo G, Graziosi C, Fauci AS| title=New concepts in the immunopathogenesis of human immunodeficiency virus infection. | journal=N Engl J Med | year= 1993 | volume= 328 | issue= 5 | pages= 327-35 | pmid=8093551 | doi=10.1056/NEJM199302043280508 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8093551  }} </ref>
 ====Clinical Latency====
@@ Line 29: / Line 29: @@
 ==Complications==
-HIV infection makes individuals highly susceptible to severe opportunistic infections and neoplastic disease.
+HIV infection makes individuals highly susceptible to severe opportunistic infections and neoplastic disease. The following complications are classically observed among patients with significant immunocompromise and rarely manifest among patients with a CD4 count greater than 350 cells/mm<sup>3</sup>.
 ===1. Infections===
-* [[Pneumocystis jirovecii]] pneumonia
+* ''[[Pneumocystis jirovecii]]'' pneumonia
 * [[Tuberculosis]]
 * Disseminated [[Mycobacterium avium complex]]
@@ Line 48: / Line 47: @@
 ===2. Cancers===
 * [[Kaposi Sarcoma]]
-* [[AIDS-related lymphoma|Non-Hodgkin's Lymphoma]]s
+* [[AIDS-related lymphoma]]s
-:*Primary CNS Lymphoma
+:*[[Non-Hodgkin's Lymphoma]]
+:*[[Hodgkin's Lymphoma]]
+:*[[Primary CNS Lymphoma]]
 :*Burkitt's Lymphoma
 :*Large B-cell Lymphoma
@@ Line 56: / Line 57: @@
 ===3. Other Complications===
-* [[HIV-associated nephropathy]]
-* [[HIV-induced pericarditis]]
+* [[HIV associated nephropathy]]
+* [[HIV induced pericarditis]]
 * HIV-associated wasting syndrome
 * [[Aortitis]]
-* [[AIDS Dementia complex]]
+* [[AIDS dementia complex]]
+* Lymphoid interstitial pneumonia
-==Coinfections==
-===Effect of Geographic Area on Opportunistic Infection===
-The opportunistic infection in AIDS patient reflect the pathogen that are common in that area.
-* In USA: Person with AIDS tends to present with commensal organism such as [[Pneumocystis pneumonia|Pneumoncystis]] and [[Candida]].
-** In a study done by National Center of HIV/AIDS,<ref name="pmid12412613">{{cite journal |author=Jones JL, Hanson DL, Dworkin MS, Alderton DL, Fleming PL, Kaplan JE, Ward J |title=Surveillance for AIDS-defining opportunistic illnesses, 1992-1997 |journal=MMWR CDC Surveill Summ |volume=48 |issue=2 |pages=1–22 |year=1999 |month=April |pmid=12412613 |doi= |url= |accessdate=2012-05-25}}</ref> PCP was the most common AIDS-defining opportunistic infection to occur first.
-*** PCP was the first OI to occur for 36% of HIV-infected persons.
-*** The most common incident AIDS-defining OI (274 cases per 1000 person-years).
-*** The most common AIDS-defining OI to have occurred during the course of AIDS (53% of persons who died with AIDS had PCP diagnosed at some time during their course of AIDS).
-* In developing nations: AIDS patients tends to present with [[Tuberculosis]], as it is more prevalent in those countries.
-===A. The Major Pulmonary Illnesses ===
-<gallery>
-Image:Pneumocystis_jiroveci.jpg|Pneumocystis jiroveci is present in this lung impression smear, using [[Giemsa stain]]
-Image:Tuberculosis_SEM.jpg|Scanning electron micrograph (SEM) of a number of [[Gram-positive]] Mycobacterium tuberculosis bacteria
- </gallery>
-====Pneumocystis jiroveci Pneumonia ====
-*Pneumocystis jiroveci pneumonia (originally known as [[Pneumocystis carinii pneumonia]], often abbreviated PCP) is relatively rare in normal, immunocompetent people but common among HIV-infected individuals. Before the advent of effective treatment and diagnosis in Western countries it was a common immediate cause of death.
-*In developing countries, it is still one of the first indications of AIDS in untested individuals, although it does not generally occur unless the CD4 count is less than 200 per µl.
-====Tuberculosis ====
-*Among infections associated with HIV, [[tuberculosis]] (TB) is unique in that it may be transmitted to immunocompetent persons via the respiratory route, is easily treatable once identified, may occur in early-stage HIV disease, and is preventable with drug therapy. However, multi-drug resistance is a potentially serious problem.
-*Even though its incidence has declined because of the use of directly observed therapy and other improved practices in Western countries, this is not the case in developing countries where HIV is most prevalent.
-*In early-stage HIV infection (CD4 count >300 cells per µl), [[TB]] typically presents as a pulmonary disease.
-*In advanced HIV infection, [[TB]] may present atypically and extrapulmonary [[TB]] is common infecting bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the central nervous system (Decker and Lazarus, 2000).
-===B. The Major Gastro-intestinal Illnesses ===
-==== Esophagitis ====
-*[[Esophagitis]] is an [[inflammation]] of the lining of the lower end of the [[esophagus]] (gullet or swallowing tube leading to the stomach). In HIV infected individuals, this could be due to fungus ([[candidiasis]]), virus ([[herpes simplex]]-1 or [[cytomegalovirus]]). In rare cases, it could be due to [[mycobacteria]] (Zaidi and Cervia, 2002).
-==== Unexplained Chronic Diarrhea ====
-*In HIV infection, there are many possible causes of [[diarrhea]], including common bacterial ([[Salmonella]], [[Shigella]], [[Listeria]], [[Campylobacter]], or [[Escherichia coli]]) and [[parasitic infections]], and uncommon [[opportunistic infections]] such as [[cryptosporidiosis]], [[microsporidiosis]], [[Mycobacterium avium complex]] (MAC) and [[cytomegalovirus]] ([[CMV]]) colitis.
-* Diarrhea may follow a course of [[antibiotics]] (common for [[Clostridium difficile]]). It may also be a side effect of several drugs used to treat HIV, or it may simply accompany HIV infection, particularly during primary HIV infection. In the later stages of HIV infection, diarrhea is thought to be a reflection of changes in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-related wasting (Guerrant et al., 1990).
-===C. The Major Neurological Illnesses ===
-==== Toxoplasmosis ====
-{| style="float:right"
-|[[Image:Toxoplasmosi_AIDS.jpg|thumb|left|Toxoplasmosis of heart in AIDS]]
-|}
-*[[Toxoplasmosis]] is a disease caused by the single-celled parasite called [[Toxoplasma gondii]]. [[Toxoplasma gondii|T. gondii]] usually infects the brain causing toxoplasma encephalitis. It can also infect and cause disease in the eyes and lungs (Luft and Chua, 2000).
-==== Progressive Multifocal Leukoencephalopathy ====
-*[[Progressive multifocal leukoencephalopathy]] ([[PML]]) is a [[demyelinating]] disease, in which the [[myelin]] sheath covering the axons of nerve cells is gradually destroyed, impairing the transmission of nerve impulses. It is caused by a virus called [[JC virus]] which occurs in 70% of the population in latent form, causing disease only when the immune system has been severly weakened, as is the case for AIDS patients. It progresses rapidly, usually causing death within months of diagnosis (Sadler and Nelson, 1997).
-==== HIV-associated Dementia ====
-*HIV-1 associated dementia ([[HAD]]) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of brain [[macrophages]] and [[microglia]] (Gray et al., 2001). These cells are actively infected with HIV and secrete [[neurotoxins]] of both host and viral origin. Specific neurologic impairments are manifested by cognitive, behavioral, and motor abnormalities that occur after years of HIV infection and is associated with low [[CD4+]] T cell levels and high plasma viral loads. Prevalence is between 15-30% in Western countries (Heaton et al., 1995; White et al., 1995) and has only been seen in 1-2% of India based infections (Satischandra et al., 2000; Wadia et al., 2001).
-===D. HIV-associated malignancies ===
-*Patients with HIV infection are susceptible to a number of malignancies (Yarchoan et al., 2005). The most common is [[Kaposi's sarcoma]], and the appearance of this tumor in young gay men in New York in 1981 was one of the first signals of the AIDS epidemic. In addition, patients with HIV infection have a higher incidence of certain high grade [[B cell lymphoma]]s, especially Burkitt-like and large cell lymphomas. These tumors, as well as aggressive cervical cancer in women, confer a diagnosis of AIDS in patients with HIV infection.
-'''AIDS-related lymphoma''' describes [[lymphoma]]s occurring in [[patient]]s with acquired immunodeficiency syndrome ([[AIDS]]).
-*A lymphoma is a type of cancer arising from [[lymphatic system|lymphoid]] [[cell (biology)|cells]]. In AIDS, the incidences of [[non-Hodgkin's lymphoma]], primary [[telencephalon|cerebral]] lymphoma and [[Hodgkin's disease]] are all increased.
-====Non-Hodgkin's Lymphoma====
-*[[Non-Hodgkin's lymphoma]] (NHL) is present in about 3% of [[HIV]] positive people at the time of their diagnosis of HIV. 20% of HIV positive patients will develop NHL.
-====Primary Cerebral Lymphoma====
-*Primary cerebral lymphoma (or ''[[primary central nervous system lymphoma]]'') is a form of NHL. It is very rare in [[immunocompetent]] people, with an incidence of 5-30 cases per million person-years. However the incidence in [[immunocompromise]]d individuals is greatly increased, up to 100 per million person-years.
-*Primary cerebral lymphoma is strongly associated with [[Epstein-Barr virus]] (EBV). The presence of EBV [[DNA]] in [[cerebrospinal fluid]] is highly suggestive of primary cerebral lymphoma.
-*Treatment of AIDS patients with [[antiretroviral drug]]s reduces the incidence of primary cerebral lymphoma.
-====Hodgkin's Disease====
-*The incidence of [[Hodgkin's disease]] in the general population is about 10-30 per million person-years. This increases to 170 per million person-years in HIV positive patients.
-===E. The Major Dermatological illnesses ===
-*AIDS-associated Kaposi sarcoma or KS-AIDS presents with cutaneous [[lesion]]s that begin as one or several red to purple-red [[macule]]s, rapidly progressing to [[papule]]s, nodules, and plaques, with a predilection for the head, neck, trunk, and [[mucous membrane]]s.
-<gallery>
-Image:Kaposi's_sarcoma.jpg|Kaposi's sarcoma lesion commonly found in patients with stage IV AIDS
-Image:Kaposi’s sarcoma intraoral AIDS 072 lores.jpg|Intraoral Kaposi’s sarcoma lesion with an overlying [[candidiasis]] infection
- </gallery>
-==Cognitive Impairment in HIV==
-'''For AIDS dementia complex , click [[AIDS dementia complex|here]]'''
-===Anatomical Areas Involved===
-*HIV is associated with pathological changes in mainly subcortical and fronto-striatal areas of the brain, including the [[basal ganglia]], deep white matter, and [[hippocampus|hippocampal]] regions.
-*Neuroimaging studies of HIV patients indicate that significant volume reductions are apparent in the frontal white matter, whereas subcortically, hypertrophy is apparent in the basal ganglia, especially the [[putamen]].<ref name = Castelo1>{{Citation |last1= Castelo |first1= JMB |last2= Courtney |first2= MG |last3= Melrose |first3= RJ |last4= Stern |first4= CE | title = Putamen hypertrophy in nondemented patients with human immunodeficiency virus infection and cognitive impairments | journal = Archives of Neurology | volume = 64| issue = 9| pages = 1275–1280 | year = 2007 | pmid = 17846265 | doi =10.1001/archneur.64.9.1275  }}</ref>
-*Some studies suggest loss of brain volume in cortical and subcortical regions even in asymptomatic HIV patients and patients who were on stable treatment.<ref name=Cohen/>  Cerebral brain volume is associated with factors related to duration of the disease and CD4 nadir; patients with a longer history of chronic HIV and higher CD4 nadir present with greater cerebral atrophy.<ref name=Cohen>{{Citation | last1 = Cohen | first1 = RA | last2 = Harezlak | first2 = J | last3 = Schifitto | first3 = G | last4 = Hana | first4 = G | last5 = Clark | first5 = U | last6 = Gongvatana | first6 = A | last7 = Paul | first7 = R | last8 = Taylor | first8 = M | last9 = Thompson | first9 = P | display-authors = 2 | title = Effects of nadir CD4 count and duration of human immunodeficiency virus infection on brain volumes in highly active antiretroviral therapy era | journal = Journal of Neurovirology | volume = 16 | issue = 1 | pages = 25–32 | year = 1981 | pmid = 20113183 | doi = 10.3109/13550280903552420 | pmc = 2995252 }}</ref>
-*CD4 lymphocyte counts have also been related to greater rates of brain tissue loss.<ref name=Cardena>{{Citation |last1= Cardenas |first1=VA|last2= Meyerhoff |first2=DJ|last3= Studholme |first3=C|last4= Kornak |first4=J|last5= Rothlind |first5=J|last6= Lampiris |first6=H|last7=Neuhaus |first7=J|last8= Grant |first8=RM|last9= Chao |first9=LL| title = Evidence for ongoing brain injury in human immunodeficiency virus-positive patients treated with antiretroviral therapy | journal = Journal of Neurovirology | volume = 15| issue = 4| pages = 324–333 | year = 2009| pmid = 19499454 | doi =10.1080/13550280902973960 |pmc= 2889153  }}</ref>
-*Current factors, such as plasma HIV RNA, have been found to be associated with brain volumes as well, especially with regards to basal ganglia volume<ref name=Cohen/> and total white matter.<ref>{{Citation | last1 =  Jernigan | first1 = TL| last2 = Archibald | first2 = SL |last3= Fennema-Notestine |first3=C|last4= Taylor |first4=MJ|last5= Theilmann |first5=RJ|last6= Julaton |first6=MD|last7= Notestine |first7=RJ|last8= Wolfson |first8=T|last9= Letendre |first9=SL| title =  Clinical factors related to brain structure in HIV: the CHARTER study | journal = Journal of Neurovirology | volume = 17| issue = 3 | pages = 248–57| year = 2011| pmid = 21544705 | doi =10.1007/s13365-011-0032-7  }}</ref>
-*Changes in the brain may be ongoing but asymptomatic, that is with minimal interference in functioning, making it difficult to diagnose HIV-associated neurocognitive disorders in the early stages.<ref name=Wang>{{Citation |last1= Wang |first1=X|last2= Foryt |first2=P|last3= Ochs |first3=R|last4= Chung |first4=JH|last5=Wu|first5=Y|last6= Parris |first6=T|last7= Ragin |first7=A| title = Abnormalities in Resting-State Functional Connectivity in Early Human Immunodeficiency Virus Infection | journal = Brain Connectivity | volume = 1| issue = | pages = 208–217 | year = 2011 | pmid = | doi =  }}</ref>
-==Behavioral Aspects of Neurocognitive Impairments==
-===Cognitive Impairments===
-*[[Cognition|Cognitive]] impairments associated with HIV occur in the domains of attention, memory, verbal fluency, and visuospatial construction. Specifically for memory, the lowered activity of the hippocampus changes the basis for memory encoding and affects mechanisms such as long-term potentiation.<ref>{{Citation |last1= Castelo |first1= JMB |last2= Sherman |first2= SJ |last3= Courtney |first3= MG |last4= Melrose |first4=RJ|last5= Stern |first5=SE| title = Altered hippocampal-prefrontal activation in HIV patients during episodic memory encoding | journal = Neurology | volume = 66| issue = 11 | pages = 1688–1695 | year = 2006| pmid = 16769942 | doi =10.1212/01.wnl.0000218305.09183.70  }}</ref>
-*Severity of impairment in different domains varies depending on whether or not a patient is being treated with [[antiretroviral drug|HAART or monotherapy]].<ref name=Cysique>{{Citation |last1= Cysique |first1= LA |last2= Maruff |first2=P|last3= Brew |first3=BJ| title = Prevalence and pattern of neuropsychological impairment in human immunodeficiency virus-infected/acquired immunodeficiency syndrome (HIV/AIDS) patients across pre-and post-highly active antiretroviral therapy eras: A combined study of two cohorts | journal = Journal of Neurovirology | volume = 10| issue = 6| pages = 350–357 | year = 2004| pmid = 15765806 | doi =10.1080/13550280490521078  }}</ref>
-*Studies have shown that patients exhibit cognitive deficits consistent with dysfunction of fronto-striatal circuits including associated parietal areas, the latter of which may account for observed deficits in visuospatial function.<ref name = Bogdanova>{{Citation |last1= Bogdanova |first1=Y|last2= Diaz-Santos |first2=M|last3= Cronin-Golomb |first3=A| title = Neurocognitive correlates of alexithymia in asymptomatic individuals with HIV | journal = Neuropsychologia | volume = 48| issue = 5| pages = 1295–1304 | year = 2010 | pmid = 20036267 | doi =10.1016/j.neuropsychologia.2009.12.033 |pmc= 2843804  }}</ref><ref name=Oleson>{{Citation |last1= Olesen |first1=PJ|last2= Schendan |first2=HE|last3= Amick |first3=MM|last4= Cronin-Golomb |first4=A| title =  HIV infection affects parietal-dependent spatial cognition: Evidence from mental rotation and hierarchical pattern perception | journal = Behavioral Neuroscience| volume = 121 | issue = 6|pages = 1163–1173 | year = 2007 | pmid = 18085869 | doi =10.1037/0735-7044.121.6.1163  }}</ref>
-===Psychological Dysfunction===
-*In addition to cognitive impairments, psychological dysfunction is also noted. For example, patients with HIV have higher rates of [[major depressive disorder|clinical depression]] and [[alexithymia]], i.e., difficulty processing or recognizing one’s own emotions.<ref name=Bogdanova/>  Patients also have more difficulty recognizing facial emotions.<ref name=Clark>{{Citation |last1= Clark |first1=US|last2= Cohen |first2=RA|last3= Westbrook |first3=ML|last4= Devlin |first4=KN|last5= Tashima |first5=KT|title = Facial emotion recognition impairments in individuals with HIV | journal = Journal of the International Neuropsychological Society | volume = 16 | issue = 6| pages = 1127–1137 | year = 2010 | pmid = 20961470 | doi =10.1017/S1355617710001037 |pmc= 3070304  }}</ref>
-*Without combination antiretroviral therapy, cognitive impairments increase with successive stages of HIV.<ref name=Heaton>{{Citation |last1= Heaton |first1=RK|last2= Franklin |first2= DR |last3= Ellis |first3=RJ|last4= McCutchan |first4=JA|last5=Letendre|first5=SL|last6=Leblanc|first6=S|last7=Corkran|first7=SH|last8=Duarte|first8=NA|last9=Clifford|first9=DB| title = HIV-associated neurocognitive disorders before and during the era of combination antiretroviral therapy: differences in rates, nature, and predictors | journal = Journal of Neurovirology | volume = 17 | issue = 1| pages = 3–16| year = 2010 | pmid = 21174240 | doi =10.1007/s13365-010-0006-1 |pmc= 3032197  }}</ref>  HIV patients in early stages show mild difficulties in concentration and attention.<ref name = Ances>{{Citation | last =  Ances | first = BM | last2 = Ellis | first2 = RJ | title =  Dementia and neurocognitive disorders due to HIV-1 infection| journal = Seminars in Neurology| volume = 27 | issue = 1 | pages = 86–92 | year = 2007 | pmid = 17226745 | doi =10.1055/s-2006-956759  }}</ref>  In advanced cases of HIV-associated dementia, speech delay, motor dysfunction, and impaired thought and behavior are observed.<ref name =Ances/> Specifically, lower motor speeds were found to correlate with hypertrophy of the right putamen.<ref name=Castelo1/>
-*The diagnosis of HIV-associated neurocognitive impairment is made using clinical criteria after considering and ruling out other possible causes.<ref name=Ances/>  The severity of neurocognitive impairment is associated with nadir CD4, suggesting that earlier treatment to prevent immunosuppression due to HIV may help prevent HIV-associated neurocognitive disorders.<ref name = Heaton/>
-==Benefits of Staging the System==
-*Easy to evaluate for new treatments
-*Define prognosis and guide patient counselling
-*Frame work for management and follow up
-*Contribute to the quality of the care of individuals who are HIV infected.
 ==Prognosis==
-Without treatment, the net median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype, and the median survival rate after diagnosis of AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months, depending on the study.<ref>{{cite paper |title= Progression and mortality of untreated HIV-positive individuals living in resource-limited settings: update of literature review and evidence synthesis |author= Zwahlen M, Egger M |url=http://data.unaids.org/pub/Periodical/2006/zwahlen_unaids_hq_05_422204_2007_en.pdf |format=PDF |date=2006 |accessdate=2008-03-19 |version= UNAIDS Obligation HQ/05/422204}}</ref> In areas where it is widely available, the development of [[HAART]] as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly-diagnosed HIV-infected person to about 20 years.<ref>{{cite journal |journal= Int J Dermatol |date=2007 |volume=46 |issue=12 |pages=1219–28 |title= Current status of HIV infection: a review for non-HIV-treating physicians |author= Knoll B, Lassmann B, Temesgen Z |pmid=18173512 |doi=10.1111/j.1365-4632.2007.03520.x |pmid=18173512}}</ref>
+Without treatment, the net median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype, and the median survival rate after diagnosis of AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months, depending on the study.<ref>{{cite paper |title= Progression and mortality of untreated HIV-positive individuals living in resource-limited settings: update of literature review and evidence synthesis |author= Zwahlen M, Egger M |url=http://data.unaids.org/pub/Periodical/2006/zwahlen_unaids_hq_05_422204_2007_en.pdf |format=PDF |date=2006 |accessdate=2008-03-19 |version= UNAIDS Obligation HQ/05/422204}}</ref> In areas where it is widely available, the development of [[HAART]] as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly-diagnosed HIV-infected person to near normal (assuming full compliance to HAART).<ref>{{cite journal |journal= Int J Dermatol |date=2007 |volume=46 |issue=12 |pages=1219–28 |title= Current status of HIV infection: a review for non-HIV-treating physicians |author= Knoll B, Lassmann B, Temesgen Z |pmid=18173512 |doi=10.1111/j.1365-4632.2007.03520.x |pmid=18173512}}</ref>
-==Related Chapters==
-*[[Immune reconstitution inflammatory syndrome]]
 ==References==
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 [[Category:Disease]]
 [[Category:Immune system disorders]]
-[[Category:Infectious disease]]
 [[category:viral diseases]]
 [[Category:Pandemics]]