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The stages and natural history of HIV infection

Author Section Editor Deputy Editor
John G Bartlett, MD Martin S Hirsch, MD Barbara H McGovern, MD

Last literature review version 18.2: Maio 2010 | This topic last updated: Janeiro 28, 2010
INTRODUCTION — The human immunodeficiency virus (HIV) pandemic has spread to every country in the world
and has infected 59 million persons worldwide, including 20 million who have already died [1]. (See "The global
human immunodeficiency virus pandemic".)

An estimated 1.1 million persons in the United States have been infected with HIV; at the end of 2003,
approximately 405,926 persons were living with AIDS. The number of reported cases in 2003 was essentially the
same as the number in 1999 [2]. This trend follows a period of sharp decline in reported cases after the
introduction of HAART.

HISTORICAL PERSPECTIVE — Since the original description in 1981 of an unusual cluster of cases of
Pneumocystis carinii pneumonia and Kaposi's sarcoma in previously healthy homosexual males, substantial
advances in our understanding of the acquired immune deficiency syndrome (AIDS) have been achieved. The
identification of a cytopathic retrovirus in 1983 and development of a diagnostic serologic test for HIV-1 in 1985
have served as the basis for developing improvements in diagnosis.

In addition, therapy was dramatically altered with the introduction of antiretroviral drugs in 1987 and
revolutionized by combination treatment, known as highly active antiretroviral therapy (HAART), in 1996. In the
three years following the introduction of HAART, mortality, AIDS, AIDS-defining diagnoses, and hospitalizations all
decreased 60 to 80 percent. The EuroSIDA study, comparing this early HAART period to pre-HAART and later
HAART (1998 to 2002) treatment periods, found a sustained decrease in mortality and progression to AIDS with
ongoing HAART [3]. Despite the absence of a cure, the natural history of the disease was radically changed [4].

Despite these advances, it is still useful to review the natural history of HIV infection without antiretroviral therapy
and the classification of disease. Although modified from the initial case definition, the newer Centers for Disease
Control and Prevention (CDC) classification system remains the cornerstone for diagnosing HIV and AIDS.

STAGES OF HIV-1 INFECTION — HIV-1 infection is divided into the following stages:

Viral transmission
Primary HIV infection (also called acute HIV infection or acute seroconversion syndrome)
Seroconversion
Clinical latent period with or without persistent generalized lymphadenopathy (PGL)
Early symptomatic HIV infection (previously known as "AIDS-related complex" or ARC and more recently
referred to as Class B according to the 1993 CDC classification)
AIDS (AIDS indicator condition according to the 1987 CDC criteria and revised 1993 CDC criteria that include a
CD4 cell count below 200/mm3 regardless of the presence or absence of symptoms)
Advanced HIV infection characterized by a CD4 cell count below 50/mm3

VIRAL TRANSMISSION — HIV infection is usually acquired through sexual intercourse, exposure to contaminated
blood, or perinatal transmission. The mode of acquiring HIV infection was undetermined in 4 percent of the cases
originally reported to the CDC. A careful review of 32,497 cases, however, revealed that only 0.2 percent had no
clearly defined risk factor. (See "Transfusion transmitted HIV infection and AIDS".)

Mode of acquisition — The distribution of the modes of transmission of HIV infection varies in different countries.
In resource-limited areas, vaginal sex is responsible for 70 to 80 percent of AIDS cases and perinatal transmission
and injection drug use (IDU) for 5 to 10 percent each [5]. In contrast, during the first 25 years of the epidemic in
the United States, male-to-male sexual contact and IDU accounted for about one-half of cases [6].

The relative contribution of different routes of transmission has varied over time in the United States as reported
by the CDC [7,8]:

The estimated number of AIDS cases remained relatively stable, but the number of cases among men who
have sex with men (MSM) and heterosexual adults and adolescents increased, while cases among injection drug
users has declined [7].

Heterosexual transmission was the most commonly reported mode of HIV acquisition among women.

A follow-up survey of 33 states found that 46 percent of new HIV diagnoses were among MSM, which
represented an increase of 8.6 percent from 2001 to 2006; declines in case finding were seen concurrently in other
risk groups (eg, high-risk heterosexuals and injection drug users) [8].

Many patients who have acquired HIV infection are unaware of their seropositive status. In the National HIV
Behavioral Surveillance (NHBS) system, cross-sectional data are collected on populations at high risk for acquiring
HIV [9]. In this ongoing study, MSM, injection drug users, and high risk heterosexuals are interviewed about their
sexual and drug-use behaviors and are offered HIV testing. Of the 1767 MSM participants to date, 450 (25
percent) tested HIV-seropositive; 217 (48 percent) were unaware of their HIV infection. Compared with MSM who
were HIV negative, MSM with unrecognized infections were less likely to have been tested during the preceding
year because they were afraid of learning they had HIV (34 versus 68 percent in HIV-negative individuals).

Minority populations are also at increased risk for HIV infection [8,10,11]. Rates of HIV infection in non-Hispanic
black females were 19 times higher than rates among non-Hispanic white females [10]. In the 2001-2006 CDC
survey noted above, approximately twice as many HIV diagnoses were made in black MSM aged 13 to 24 years
compared with white MSM [8].

Risk factors — Risk factors for HIV transmission include viral load, lack of circumcision, sexual risk, presence of
ulcerative sexually transmitted diseases, nitrate inhalant use, and host and genetic factors [12-14].

Viral load — The influence of viral load in relation to other potential risk factors for heterosexual transmission
of HIV was examined in a prospective study of 415 Ugandan couples with discordant HIV serostatus [12]. Over a
30 month follow-up period, 90 patients seroconverted (21.7 percent). The following findings were noted:

The efficiency of transmission was approximately the same for female to male as for male to female.

The mean viral load was significantly higher in those who transmitted HIV to their partner (90,254 compared to
38,029 copies/mL). Furthermore, there were no cases of transmission among the 51 subjects with HIV RNA levels
less than 1500 copies/mL.

A dose response relationship of increased transmission with increased viral load was defined. In multivariate
analysis, each log increment in the viral load was associated with a rate ratio of 2.45 for seroconversion.

The importance of viral load is also underscored by mathematical models that suggest that a large proportion of
HIV infections may be transmitted by individuals with primary infection [15]. This is probably related to the high
levels of viremia that are seen in the setting of acute infection. (See "Primary HIV-1 infection: Diagnosis and
treatment", section on 'Viral load'.)

Sexually transmitted diseases — The presence of sexually transmitted diseases also increases the risk of HIV
acquisition as demonstrated in a study of 174 monogamous Ugandan couples with discordant HIV serostatus
[15,16]. The probability of transmission was approximately four times higher in patients with genital ulceration
compared to those without. Multiple other studies have confirmed these results. (See "Epidemiology, clinical
manifestations, and diagnosis of genital herpes simplex virus infection" and "Epidemiology, clinical presentation,
and diagnosis of syphilis in the HIV-infected patient".)

Sexual risk — In a study that enrolled 3257 MSM in six US cities from 1995 to 1997, risk factors for HIV
seroconversion included history of a large number of sexual partners, unprotected receptive anal sex with a partner
with an unknown HIV serostatus, and use of nitrate inhalants [17].

There are few studies documenting oral transmission of HIV infection; this could reflect low titers of infectious virus
in saliva [18].

Lack of circumcision — Lack of circumcision is associated with risk of HIV transmission in cohorts of
heterosexual couples and MSM [12,17].

Genetic background — Similarity of HLA-class-I alleles (see "Human leukocyte antigens (HLA): A roadmap")
between HIV discordant couples may affect the risk of transmission, by selecting for viral strains that are more
likely to escape the immune containment of the seronegative partner. In a study of 125 initially serodiscordant
couples with intracouple transmission, and 104 persistently serodiscordant couples, sharing of HLA-B alleles was
associated with accelerated intracouple transmission of HIV after controlling for other variables (hazard ratio 2.23,
95% CI 1.52 to 3.26) [14].

PRIMARY HIV INFECTION — Symptomatic primary HIV infection occurs in many patients and has been reported
in all major risk categories. The topic of primary HIV infection is discussed in detail elsewhere. Only issues related
to primary infection and its impact on the natural history of HIV will be discussed here. (See "Primary HIV-1
infection: Pathogenesis; epidemiology and clinical manifestations".)

Symptoms and disease progression — The presence of symptoms and a prolonged illness (>14 days) appears
to correlate with more rapid progression to AIDS [19,20]. In one study, for example, the risk of progression to an
AIDS-defining diagnosis within three years following seroconversion was substantially higher in those with acute
symptoms lasting more than 14 days than in those who were asymptomatic or had only mild symptoms (78 versus
10 percent) [19].
Level of viremia at seroconversion — Following HIV seroconversion, there is marked variability in disease
progression, in the absence of antiretroviral therapy [21,22]. In a 1995 study of 62 MSM with documented HIV
seroconversion, a plasma HIV RNA level greater than 1 x 10(5) Eq/mL was the most powerful predictor of AIDS
over time (OR 10.8) [21]. The persistence of detectable HIV RNA in plasma after primary HIV infection was
associated with the development of AIDS and significant CD4 T cell count declines. In a prospective study of 218
female sex workers in Kenya with a median duration of follow-up of 4.6 years, higher set point viremia, lower
early CD4 T cell counts, and symptomatic primary HIV infection predicted faster progression to death [22].

After approximately six months of infection, plasma viremia reaches a steady state level; cytotoxic CD8 T cells play
a critical role in achieving that equilibrium and preventing further decline in the CD4 cell compartment [23,24]. In
a prospective study of 33 patients with primary HIV-1 infection, those with higher frequencies of Env-specific
memory CTLs had median levels of plasma HIV-1 RNA only about one-third that of patients with lower frequencies
and had a lower likelihood of progression to a CD4 cell count below 300/mm3 at 18 months (20 versus 56
percent) [24].

The topic of primary HIV infection is discussed in detail elsewhere. (See "Primary HIV-1 infection: Pathogenesis;
epidemiology and clinical manifestations".)

SEROCONVERSION — Most patients seroconvert to positive HIV serology within 4 to 10 weeks after exposure
using newer diagnostic tests, and !95 percent seroconvert within six months [25-27]. The median time from
exposure to positive serology in one study was 63 days [28]. (See "Primary HIV-1 infection: Diagnosis and
treatment".)

A small proportion of seroconverters demonstrate significant immune responses and virologic control early in
infection. In an analysis of 2176 patients with documented HIV seroconversion, 145 patients (7 percent)
spontaneously controlled viremia [29]. Women, and those without symptoms at seroconversion, were more likely
to achieve a non-detectable HIV RNA. Such virologic control may have a profound effect on the natural history of
HIV infection. (See 'Long-term nonprogressors' below.)

CLINICAL LATENT PERIOD — The period of early HIV disease extends from seroconversion to six months
following HIV transmission. During the period of asymptomatic infection, patients generally have no findings on
physical examination except for possible lymphadenopathy. "Persistent generalized lymphadenopathy" (PGL) is
defined as enlarged lymph nodes involving at least two noncontiguous sites other than inguinal nodes. Studies of
the lymph nodes at this stage reveal high concentrations of extracellular HIV on the follicular dendritic cell
processes within germinal centers and intracellular HIV predominantly in its latent form [30].

The lymphoid tissue serves as the major reservoir for HIV. The follicular dendritic cells in lymphoid tissue filter and
trap free virus and infected CD4 T cells. The viral burden in peripheral blood mononuclear cells is relatively low at
this time. The lymph node architecture is disrupted and more HIV is released peripherally into the bloodstream as
the disease progresses.

Viral dynamics — Virologic studies in patients with asymptomatic HIV infection show high rates of HIV replication
and destruction of an average of 10(9) CD4 cells daily [31,32]. Cell death and replacement are in near balance
during this phase of the illness; thus, a relatively steady state of cell counts and viral load is achieved despite
remarkably high turnover rates of HIV and CD4 cells. As an example, the HIV RNA levels are usually stable over
time with only rare changes exceeding 1 log [33].

The half-life of HIV in serum is approximately 1.2 days, about 24 hours intracellularly, and about 6 hours as
extracellular virus. About 30 percent of the total body viral burden is turned over daily. Furthermore, 6 to 7
percent of the total CD4 cells turnover each day, and the entire supply of CD4 cells turns over every 15 days. The
implication of these observations is that "AIDS is primarily a consequence of continuous, high-level replication of
HIV-1, leading to virus and immune-mediated killing of CD4 lymphocytes" [32].

This "set point" in the viral load and the CD4 count correlates with prognosis [34,35]. Viral load is the most
important predictor of progressive disease in early stages of HIV infection while the CD4 count is an important
prognosticator in late stage disease [36].

CD4 T cell dynamics — Clinical studies show considerable variation between patients in CD4 cell count and viral
burden during this period [37]. The viral load stabilizes at six months and often remains at the same level or
increases slowly (0.15 percent per week in one series) for a few years in the absence of antiretroviral therapy [34].

Population-based studies of the natural history of HIV infection in MSM show that the mean CD4 count prior to
seroconversion is 1000/mm3. The count decreases to a mean of 780/mm3 at six months post-seroconversion and
to 670/mm3 at one year [38]. However, some patients have a substantially lower CD4 count at one year [37,39].

The rapid decline in CD4 cells in the early stages of HIV
CD4 cells from the peripheral blood to lymphatic tissue.
about 50/mm3 per year, with a range of 30 to 90/mm3
decline correlates with the viral burden, which averaged
one study [44].
infection may reflect destruction of CD4 cells or a shift of
After one year, the rate of CD4 cell decline averages
per year [34,38,40-43]. As expected, the rate of CD4 cell
a decrease of 4 percent per log10 copies/mL per year in
A subset of patients has sustained high levels of CD4 cells. The term "chronic nonprogressor" is sometimes used in
reference to these patients. (See 'Long-term nonprogressors' below.)

EARLY SYMPTOMATIC HIV INFECTION — The stage of early symptomatic HIV infection is also called "Class B"
according to the CDC 1993 classification system and was formerly called "AIDS-related complex". Examples of
Class B conditions are shown in Table 2 (table 1). Although these diseases occur in association with many
disorders, they are more frequent and more severe when associated with HIV infection. The B conditions are
not AIDS-indicator conditions.

AIDS — The definition of AIDS has evolved since the beginning of the epidemic.

The 1987 definition of AIDS included conditions indicative of severe immunosuppression, especially defective cell-
mediated immunity [45]. The subsequent revised CDC classification has three ranges of CD4 cell counts and uses
a matrix of nine mutually exclusive categories (table 2).

The 1993 definition of AIDS includes all of the AIDS-indicator diseases in the 1987 version with three additions:
recurrent bacterial pneumonia; invasive cervical cancer; and pulmonary tuberculosis (table 3). The most
substantive change in the classification was the inclusion of all patients with a CD4 cell count below 200/mm3
regardless of the presence or absence of symptoms.

Using data from the Multicenter AIDS Cohort Study, the median CD4 count at the time of an AIDS-defining
complication was 67 cells/mm3 [46]. However, approximately 10 percent of patients develop an AIDS-defining
diagnosis with a CD4 count above 200/mm3.

The median time from the onset of severe immunosuppression (defined as a CD4 cell count below 200/mm3) to an
AIDS-defining diagnosis (1987 criteria) is 12 to 18 months in persons not receiving antiretroviral treatment [47].

As with depletion of CD4 T cells, humoral immunity wanes over time. B cells exhibit increased expression of
markers of activation and proliferation [48]. In addition, in advanced HIV infection, B cells undergo terminal
differentiation leading to increased immunoglobulin secretion [49]. This may lead to a polyclonal
hypergammaglobulinemia; however, many of these antibodies are non-specific. This may explain the paradox
between high circulating levels of immunoglobulins and an increased risk of bacterial infections (eg, recurrent
pneumonia) that occurs in late-stage AIDS. Humoral immunity generally improves dramatically after the initiation
of antiretroviral therapy. (See "When to initiate antiretroviral therapy in HIV-infected patients".)

Conditions that define an AIDS diagnosis — Prior to the HAART era, the CDC reported 71,704 new cases in the
1997 fiscal year. The following was the rank order of first AIDS-defining conditions in the CDC Adult/Adolescent
Spectrum of HIV Disease Sentinel Surveillance Project [50]:

P. carinii pneumonia — 42.6 percent

Esophageal candidiasis - 15.0 percent
Wasting — 10.7 percent
Kaposi's sarcoma — 10.7 percent
Disseminated M. avium infection — 4.8 percent
Tuberculosis — 4.5 percent
Cytomegalovirus disease — 3.7 percent
HIV-associated dementia — 3.6 percent
Recurrent bacterial pneumonia — 3.0 percent
Toxoplasmosis — 2.6 percent
Immunoblastic lymphoma - 1.9 percent
Chronic cryptosporidiosis - 1.5 percent
Burkitt lymphoma - 1.5 percent
Disseminated histoplasmosis - 1.0 percent
Invasive cervical cancer - 0.9 percent
Chronic Herpes simplex — 0.5 percent

Advanced HIV infection — Patients with advanced HIV infection have a CD4 cell count below 50/mm3. Their
median survival is 12 to 18 months in the absence of antiretroviral therapy [51-53]. Virtually all patients who die
of HIV-related complications have CD4 cell counts in this range.

LONG-TERM NONPROGRESSORS — Some patients exhibit remarkable clinical stability and remain asymptomatic
over many years without antiretroviral therapy [42,54-56]. These patients are called "long-term nonprogressors,"
which is arbitrarily defined as HIV infection for at least 13 years, no antiretroviral agents, lack of symptoms, CD4
count above 600/mm3, and no decrease in CD4 count for more than five years. Large longitudinal studies show
that 4 to 7 percent of HIV-infected patients satisfy these criteria and this reflects to a large extent a robust
cytotoxic T cell response and preservation of lymph node architecture [43,44].

A review of the experience in the MACS data suggests that 13 percent of MSM infected at a young age will remain
asymptomatic for more than 20 years without antiretroviral therapy [31]. Similar results have been noted in
persons with hemophilia [32]. The main correlate with delayed progression is low viral burden that probably
reflects an effective immunologic response with HIV-specific CD4 T cells early in the course of infection [33].
ELITE CONTROLLERS — "Elite controllers" are HIV-seropositive individuals who have no evidence of viremia, as
measured by ultrasensitive assays (either <50 or <75 copies/mL), and maintain high CD4 cell counts. These
patients represent a small minority of HIV-infected individuals (1/300 patients) and the mechanisms that lead to
spontaneous virologic control without treatment are unknown. Some studies suggest that host factors may play a
role in the control of viral replication, whereas others suggest infection with defective HIV variants [57].

In elite controllers, viral load suppression has been observed to be comparable to that seen in patients who are
taking potent combination antiretroviral therapy [58]. One study evaluated cellular and humoral immune responses
and host genetics in 64 elite controllers, 50 persons with low levels of detectable viremia (<2000 copies/mL,
"viremic controllers"), and patients with progressive infection [59]. The following findings were noted:

The HIV gag protein was preferentially targeted by CD8 T-cell responses in elite and viremic controllers
compared to patients with progressive infection.

The elite controller group had a higher frequency of HIV-specific CD4 and CD8 T-cells producing interferon
gamma and interleukin-2 and a paucity of broadly cross-reactive neutralizing antibodies compared to the other two
groups.

Compared to prior studies, the majority of HIV controllers did not carry HLA-B*57 or specific chemokine
polymorphisms associated with slower disease progression. In another case study of an HIV transmission pair,
both of whom were HLA-B*57-positive, the transmitter progressed to AIDS while the recipient became an elite
controller [57]. While compensatory mutations occurred in viral isolates from the patient with AIDS, the elite
controller had superior HIV-specific CD8 T-cell responses that were associated with viral suppression. These results
suggest that there remain undefined viral or host factors that contribute to this unique disease phenotype. (See
"Factors affecting HIV progression".)

Further studies, including viral and host genetic analyses, are underway in the International HIV Controllers Study
that seeks to enroll 1000 elite controllers and 1000 viremic controllers. A fundamental understanding of these
groups may be an important advance in vaccine research. More information regarding this study is available at
www.hivcontrollers.org.

Other clinical studies on this patient population are also being performed through the National Institutes of Health
(http://clinicaltrials.gov/ct2/results?term=long-term+non+progressors&fund=0), the AIDS Research Alliance (310-
358-2429), and within major cities in the United States (eg, San Francisco;
http://ari.ucsf.edu/programs/elite.aspx).

SUMMARY

HIV-1 infection is divided into stages of primary infection with seroconversion, clinical latency, early
symptomatic disease, and AIDS. The mode of acquisition is mainly through heterosexual transmission in
developing countries; in the United States, men who have sex with men (MSM) and persons exposed through
heterosexual contact account for the majority of HIV/AIDS diagnoses. Risk factors for transmission include high
plasma HIV viral load and presence of ulcerative genital sexually transmitted diseases. (See 'viral
transmission' above.)

Symptomatic primary HIV infection occurs in many patients and has been reported in all major risk categories.
The presence of symptoms and a prolonged illness correlates with more rapid progression to AIDS. The period of
early HIV disease extends from seroconversion to six months following HIV transmission. (See 'Primary HIV
infection' above.)

During the period of asymptomatic infection, patients generally have no findings on physical examination except
for lymphadenopathy. Despite the lack of symptoms, high rates of HIV replication and CD4 T cell destruction may
be occurring. (See 'Clinical latent period' above.)

The stage of early symptomatic HIV infection is called "Class B" according to the CDC 1993 classification
system and was formerly called "AIDS-related complex". The most substantive change in the classification system
was the inclusion of all patients with a CD4 cell count below 200/mm3 as having AIDS, regardless of the presence
or absence of symptoms. (See 'Early symptomatic HIV infection' above.)

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GRAPHICS
Examples of B conditions in early symptomatic HIV infection

Thrush

Vaginal candidiasis that is persistent, frequent, or difficult to manage

Oral hairy leukoplakia

Herpes zoster involving two episodes or more than one dermatome

Peripheral neuropathy

Bacillary angiomatosis

Cervical dysplasia

Cervical carcinoma in situ

Constitutional symptoms such as fever (38.5°C) or diarrhea for more than one month

Idiopathic thrombocytopenic purpura

Pelvic inflammatory disease, especially if complicated by a tubo-ovarian abscess

Listeriosis
AIDS surveillance case definitions

Clinical categories
CD4 cell A- Asymptomatic, PGL or acute B*- Symptomatic C- AIDS indicator
categories HIV infection (not A or C) condition (1987)

>500/mm3 (!29 A1 B1 C1
percent)

200-499/mm3 (14- A2 B2 C2
28 percent)

<200/mm3 (<14 A3 B3 C3
percent)

1993 AIDS surveillance case definition for adolescents and adults. All patients in
categories A3, B3, C1-C3 are reported as AIDS based upon prior AIDS-indicator conditions
and/or a CD4 cell count <200/mm3. AIDS-indicator conditions include three new entries
added to the 1987 case definition: recurrent bacterial pneumonia, invasive cervical cancer,
and pulmonary tuberculosis. * Symptomatic conditions not included in category C that (a) are
attributed to HIV infection or indicate a defect in cell-mediated immunity or (b) are conditions considered to
have a clinical course or to require management that is complicated by HIV infection. Examples of B
conditions include but are not limited to baciliary angiomatosis; thrush; vulvovaginal candidiasis that is
persistent, frequent or poorly responsive to therapy; cervical dysplasia (moderate or severe); cervical
carcinoma in situ; constitutional symptoms such as fever (38.5°C) or diarrhea for more than one month;
oral hairy leukoplakia; and herpes zoster involving two episodes or more than one dermatome. Data from
MMWR Morb Mortal Wkly Rep 1992; 41:1.
 Indicator conditions in case definition of AIDS

Candidiasis of esophagus, trachea, bronchi, or lungs

Cervical cancer, invasive*•

Coccidioidomycosis, extrapulmonary*

Cryptococcosis, extrapulmonary

Cryptosporidiosis with diarrhea for >1 month

Cytomegalovirus of any organ other than liver, spleen, or lymph nodes

Herpes simplex with mucocutaneous ulcer for >1 month or bronchitis, pneumonitis, esophagitis

Histoplasmosis, extrapulmonary*

HIV-associated dementia: disabling cognitive and/or motor dysfunction interfering with occupation or activities
of daily living

HIV-associated wasting*: involuntary weight loss of >10 percent of baseline plus chronic diarrhea (!2 loose
stools/day for !30 days) or chronic weakness and documented enigmatic fever for !30 days

Isosporosis with diarrhea for >1 month*

Kaposi's sarcoma in patient younger than age 60 (or older than age 60*)

Lymphoma of brain in patient younger than age 60 (or older than age 60*)

Lymphoma, non-Hodgkin's of B cell or unknown immunologic phenotype and histology showing small,
noncleaved lymphoma or immunoblastic sarcoma

Mycobacterium avium or M. kansasii, disseminated

Mycobacterium tuberculosis, disseminated*

Mycobacterium tuberculosis, pulmonary*•

Nocardiosis*

Pneumocystis carinii (P jiroveci) pneumonia

Pneumonia, recurrent-bacteria*•

Progressive multifocal leukoencephalopathy

Salmonella septicemia (nontyphoid), recurrent*

Strongyloidosis, extraintestinal

Toxoplasmosis of internal organ

* Requires positive HIV serology.

• Added in the revised case definition 1993.

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