Human immunodeficiency virus infection

Last updated: November 2, 2023

Summarytoggle arrow icon

Infection with the human immunodeficiency virus (HIV) leads to a complex disease pattern that ultimately results in chronic immunodeficiency. HIV can be transmitted sexually, parenterally, or vertically (e.g., peripartum from mother to child). Infection is most common in the young adult population between 20 and 30 years of age. The virus infects macrophages and other CD4+ cells, leading to the destruction of CD4 T cells, which are one of the key mechanisms of cellular immune defense. The three major stages of HIV infection are acute infection, clinical latency, and acquired immunodeficiency syndrome (AIDS). Detailed classifications of clinical staging have been established by the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO). During the acute infection stage, the virus reproduces rapidly in the body, which can lead to the onset of acute, nonspecific (e.g., flu-like) symptoms, also known as acute retroviral syndrome (ARS), within 2–4 weeks. However, approximately half of all infected individuals remain asymptomatic. Once the acute infection stage subsides, the clinical latency stage begins. As with the acute infection stage, many individuals remain asymptomatic during this period while others develop non-AIDS-defining conditions (e.g., oral hairy leukoplakia). The last stage, AIDS, is characterized by AIDS-defining conditions, such as Kaposi sarcoma, and/or a CD4 count < 200 cells/mm3.

HIV infection can be reliably detected using antigen/antibody-based tests. In patients with confirmed infection, treatment with a combination of antiretroviral medications (ART) is started as soon as possible. The effectiveness of the treatment is monitored via regular checks of CD4 count and viral load. Patients in the advanced stages of HIV infection may additionally require treatment of HIV-associated conditions and prophylaxis for opportunistic infections. Significant advances in treatment mean that the average life expectancy of HIV patients receiving ART is approaching that of the general population. Partners of HIV-positive people and individuals at high risk of HIV infection can reduce the risk of contracting the infection by taking ART prior to exposure (preexposure prophylaxis) or following exposure (postexposure prophylaxis) to the virus.

Epidemiologytoggle arrow icon

  • Incidence (in the US)
    • HIV infection: peak incidence between ages 20 and 30 (∼ 35/100,000)
    • AIDS: peak incidence approx. age 45 (∼ 14/100,000)
    • Ethnicity: Incidence is significantly higher in the Black population than in other population groups.
  • Prevalence
    • US: ∼ 1.2 million
    • Global: ∼ 37 million


Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

Pathogen (human immunodeficiency virus)

  • Family: Retroviridae
  • Genus: Lentivirus
  • Species
    • HIV-1: most common species worldwide
    • HIV-2: restricted almost completely to West Africa
  • Structure: icosahedral with a conical capsid and a spiked envelope
  • Genome
    • Pseudodiploid (2 RNA molecules yielding 1 DNA molecule)
    • 9 genes encoding a total of 15 proteins
  • Function of structural proteins
    • pol gene codes for a polyprotein which consists of
      • Protease: cleavage of gag and gag-pol proteins during maturation of the virion [4]
      • Reverse transcriptase: converts viral RNA to dsDNA
      • Integrase: helps insert the viral genes into the host genome
    • gag gene codes for gag protein, which consists of
    • env gene codes for gp160 which gets cleaved into envelope glycoproteins
      • gp120: attaches to host CD4+ T-cells
      • gp41: assists in fusion and entry of the virus into the host cell
    • tat gene (trans-activator of transcription) codes for tat protein which promotes viral transcription
    • rev gene: codes for the rev protein, which regulates translocation of unspliced and incompletely spliced mRNAs

Polly is a Really Important Person.”: the proteins coded by the pol gene are Reverse transcriptase, Integrase, and Protease.

Routes of transmission

Risk of transmission can be lowered significantly if HIV infection is treated consistently and viral load is below the limit of detection.


Pathophysiologytoggle arrow icon

Natural history of HIV infection

Viral load predicts the rate of disease progression and CD4 count correlates with immune function.

Acute HIV syndrome does not develop in all patients. Absence of symptoms may delay diagnosis.

The role of immune response

  • Because HIV infects cells of the immune system itself, activation of cellular immunity is a factor that paradoxically helps the virus spread and ensures chronic persistence of the infection.
  • HIV evades immune control via:
    • Genetic mutation and recombination
    • Downregulation of MHC class I surface molecules in infected cells


Clinical featurestoggle arrow icon

General considerations

  • There are no clinical features specific to HIV infection
  • In early HIV infection, patients are often asymptomatic.
  • Incubation period: usually 2–4 weeks [12]
  • Infectiousness: two peaks (1st peak: within the first months after infection; 2nd peak: during AIDS-stage)

Acute HIV infection [8][13]

Clinical latency and AIDS

Test patients with a history of intravenous drug use who present with otherwise unexplained weight loss, depression, and/or dementia for HIV.

Unlike oral candidiasis, esophageal candidiasis is an AIDS-defining condition.


Stagestoggle arrow icon

CDC classification system for HIV [14]

  • CDC categories of HIV are based on CD4 count in combination with current or previously diagnosed HIV-related conditions.
  • Any patient belonging in categories A3, B3 or C1-C3 is considered to have AIDS.
CD4 cell count category
(normal cell count: 500–1500 cells/mm3)

Clinical category A

Asymptomatic, Acute HIV
or PGL

Clinical category B

Symptomatic conditions,
not A or C

Clinical category C

AIDS-defining conditions

(1) ≥ 500 cells/mm3 A1 B1 C1
(2) 200–499 cells/mm3 A2 B2 C2
(3) < 200 cells/mm3 A3 B3 C3

PGL= Persistent generalized lymphadenopathy

WHO (World Health Organization) classification [15]

WHO classifies individuals with confirmed HIV infection according to clinical features and diagnostic findings:

Diagnosticstoggle arrow icon

Approach [16]

Specific screening and testing strategies depend on local factors including regional prevalence and testing capabilities.

Overview of tests and methods [16]

Serological assays

Serological assays are commonly used for both screening and diagnosis and may detect HIV antigen, antibodies, or both.

Comparison of HIV serological assays [16][21]
Generation Test characteristics
First-generation HIV test
  • Detects IgG only
  • Cannot differentiate between HIV-1 and HIV-2 infection
  • Sensitive but not very specific
Second-generation HIV test
Third-generation HIV test
  • Detects IgG and IgM
  • Cannot differentiate between HIV-1 and HIV-2 infection
  • More sensitive and specific
Fourth-generation HIV test
Fifth-generation HIV test [21]

Virological testing [23]

Virological tests are most commonly used for screening infants and confirmation of disease in both infants and adults.

Screening and diagnosis

Recommended laboratory-based HIV studies [23][24]
Age Preferred test
Screening Adults and children ≥ 18 months
Infants < 18 months
Confirmation Adults and children > 24 months
Infants ≤ 24 months

Indications for HIV testing [18][19]

HIV testing should be offered to patients who have signs that raise concern for HIV infection, prior exposure, and as part of routine screening.

  • Routine screening
    • All individuals > 13 years of age in all health care settings [19][25]
    • Any individuals (even if previously tested):
    • One-time testing is recommended early in all pregnancies
  • Targeted testing

In most US states, HIV testing requires patient consent (opt-out); in the majority of locations, oral consent is sufficient, but check local guidance.

Screening studies [24]

A negative combination antibody/antigen test two weeks after exposure essentially rules out HIV infection (almost 100% sensitivity).

If the result of a rapid test is positive, a laboratory-based screening test should be sent, followed by confirmatory testing if appropriate. [24]

Confirmatory studies

Additional evaluation for patients with newly diagnosed HIV [30][31]

Assessment of organ function

Assessing organ function is important to screen for HIV-associated complications, establish a baseline in order to monitor toxicity, and help select an ART regimen.

Advanced HIV studies

The following studies are recommended to screen for drug resistance, assist in the selection of an appropriate ART regimen, and establish a baseline to monitor the efficacy of therapy.

  • HIV drug resistance testing: Genotypic assays are preferred over phenotypic assays. [30][32]
  • CD4+ count: correlates with overall immune function ; [31]
    • Normal values are > 500 cells/mm3, whereas in the advanced stages of HIV the CD4+ count is often < 200 cells/mm3.
    • Critical measurement to determine when to initiate opportunistic infection prophylaxis
    • CD4+ counts increase in response to successful ART therapy.
  • Viral RNA load: indicator of ART response
    • Decrease in viral loads indicates effective treatment.
    • Prognostic marker in long-term treatment (higher viral load → ↑ destruction of CD4+ lymphocytes more severe immunodeficiency worse prognosis) [33]
  • CD4 cell percentage: used for the assessment of immune function and less variable than CD4+ count [31]
    • Preferred for monitoring children < 5 years of age, as absolute CD4+ count varies more than in adults
    • Values of 14–29% are equivalent to a CD4+ count of 200–500 cells/mm3.
  • CD4:CD8 ratios (no longer routinely recommended): an increase in the ratio following ART initiation suggests improved immune system functioning

Measurement of CD8 cell count and CD4:CD8 ratios is not routinely recommended, as the results are not used to guide treatment. [31]

Screening for associated complications

To identify any AIDS-defining illnesses and coinfection with other bloodborne viruses or STIs.

Managementtoggle arrow icon

General principles [30][34]

Early treatment is particularly critical in patients with a low CD4 count (< 350 cells/mm3), high viral load, or an AIDS-defining illness.

Adherence to ART can be improved by considering social determinants of health and addressing modifiable factors such as comorbid mental illness or substance use disorder, unstable housing, and barriers to attending regular clinic visits. [30]

In the US, HIV/AIDS is a notifiable disease in every state.

Antiretroviral therapytoggle arrow icon

  • Start ART as soon as possible to prevent further progression of the disease. [30]
  • Factors to consider when selecting a regimen include: [30]

Initiation of ART should be delayed in the setting of TB meningitis and cryptococcal meningitis because of the high risk of immune reconstitution syndrome!

Initiation of treatment should not be delayed to await results of advanced HIV studies, e.g., drug resistance or hepatitis screening.

Initial ART regimens [30]

Recommended initial regimens [30]
Regimen Recommended drug combinations Combination tablet Indications/contraindications
  • Biktarvy®
  • May be used for immediate treatment in individuals for whom advanced HIV studies are not yet available and whose hepatitis B status is unknown
  • Triumeq®
  • May be used in pregnancy [23]
  • Contraindicated in patients who are HLA-B*5701 positive
  • Dovato®

Do not use abacavir-containing regimens for patients with an unknown or positive HLA-B*5701 status, because of the risk of abacavir hypersensitivity reaction!

When available, use combination tablets to reduce pill burden and improve adherence. [35]

Special considerations

Stopping NRTIs in patients with hepatitis B co-infection can lead to an acute worsening of their hepatitis!

Overview of antiretroviral drugs [30][37][38]

Nucleoside reverse transcriptase inhibitors (NRTIs)

Most NRTIs end in “-ine,” protease inhibitors in “-navir,” and integrase inhibitors in “-gravir.”

“The nuclear plant is in the vuds (read: “woods”)”: Nucleoside reverse transcriptase inhibitors end in “-vudine.”

Nonnucleoside reverse-transcriptase inhibitors (NNRTIs)

HIV protease inhibitors (PIs)

Subtherapeutic doses of ritonavir can be used to increase concentrations of other HIV drugs because it is a cytochrome P450 inhibitor. [53]

Integrase inhibitors (INIs or InSTIs)

  • Medications in class
    • Bictegravir
    • Cabotegravir
    • Dolutegravir
    • Elvitegravir
    • Raltegravir
  • Mechanism of action: inhibition of the viral integrase → blockade of viral DNA integration into the host's DNA → inhibition of viral replication [37]
  • General adverse effects [40][41]
    • Rash
    • Hypersensitivity syndrome in rare cases
  • Additional medication-specific adverse effects: : muscle inflammation causing elevated creatinine kinase : raltegravir, dolutegravir [40][41]

An intramuscular injection consisting of cabotegravir and rilpivirine can be used for patients whose HIV is well controlled on oral ART but it should not be used as an initial regimen.

Entry inhibitors [54]

Enfuvirtide provides defusion of viral fusion.”

“Maraviroc will block the viral dock.”

Monitoring antiretroviral therapytoggle arrow icon

The treatment response of patients with HIV who are on ART should be frequently monitored by assessing their CD4+ count and HIV viral load. Any concerns regarding the failure of treatment should be referred to the infectious disease service. [30]

Monitoring studies [56]

Frequency of monitoring studies [56]
Frequency of test Test

4–8 weeks after initiation of ART

Every 3–6 months
Every 6 months
Every 12 months

Patients should have monitoring studies performed more frequently if clinically indicated or in treatment failure!

Virological failure [30]

  • Definition: the inability to maintain or achieve viral levels of < 200 copies/mL
  • Causes: patient-related factors (e.g., poor drug adherence, cost), HIV-related factors (e.g., drug resistance, high pretreatment viral load), ART-related factors (e.g., drug interactions, suboptimal pharmacokinetics)
  • Management: Address any identifiable cause of failure and adjust ART regimen if indicated.

Poor CD4 count recovery [30]

  • Definition: CD4+ counts remain persistently low (< 500, although effects are most concerning if CD4 remains < 200) despite adequate suppressive ART. These individuals have increased morbidity and mortality.
  • Causes: medication side effects, co-infections such as HIV-2 and HCV, other medical problems such as malignancy
  • Management: Identify modifiable causes of CD4 cell lymphopenia. Changing or adding antiretrovirals is not recommended.

Preventative health caretoggle arrow icon

Opportunistic infections [57][58]

Immunizations [58]

Some live vaccinations, e.g., the MMR, should not be given until CD4 count is ≥ 200; consult with an infectious disease specialist before giving vaccinations to patients with low CD4 counts. [58]


Risk reduction

Screening [59]

HPV cotesting at the time of a pap smear is not recommended for patients < 30 years of age because of the high prevalence of infection in this age group, which typically self-resolves.

Complicationstoggle arrow icon

Patients who start ART are at risk of developing complications related to the recovery of their immune system. Complications relating to immunocompromise (especially if CD4 levels are < 200) and/or HIV infection itself may also be seen (see “HIV-associated conditions).

Immune reconstitution inflammatory syndrome (IRIS) [60][61]

  • Definition: an inflammatory syndrome that can occur after initiation of ART and consists of either the appearance of a new condition or worsening of a preexisting condition
  • Epidemiology: common; occurs in ∼ 15–25% of patients starting ART [62]
  • Etiology: believed to result from the restoration of the immune system and its response to antigenic stimulation. The stimulus may be: [60]
  • Risk factors [60]
  • Clinical presentation [61]
    • Develops within 4–8 weeks of initiation of ART
    • Presentation varies depending on the underlying illness, however, patients often have clinical deterioration and localized tissue inflammation.
  • Diagnosis is clinical and based on presence of the following: : [63]
    • Symptoms cannot be explained by the expected clinical course of a known infection, a drug side-effect, or a new infection.
    • Symptoms of an infectious or inflammatory (e.g., autoimmune) condition
    • Treatment with effective ART (defined by a significant decrease in HIV viral RNA or an increase in CD4 count)
    • HIV diagnosis
  • Management [61]
    • Provide supportive care and continue treatment of the associated condition, e.g., with antibiotics, chemotherapy.
    • Do not interrupt ART except in severe, life-threatening IRIS.
    • Consider corticosteroids (e.g., prednisone [61]) for severe IRIS depending on the underlying cause.
  • Prevention

Corticosteroids should not be given to prevent IRIS, nor should they be used to manage IRIS caused by Kaposi sarcoma or cryptococcal meningitis! [61]

We list the most important complications. The selection is not exhaustive.

Prognosistoggle arrow icon

  • Morbidity and mortality among patient subsets
    • Untreated, HIV leads to death on average 8–10 years after infection.
    • Progression varies among individuals: Some patients may die within a few years while others can remain asymptomatic for decades.
      • Untreated individuals with advanced HIV infection usually die within a few years (median survival is 12–18 months).
        • Some untreated individuals show only slow progression and can remain asymptomatic for more than 20 years.
        • In rare cases, untreated individuals have no detectable viremia and continue to have high CD4 counts for long periods.
    • The average life expectancy of HIV-infected individuals who receive adequate antiretroviral treatment is approaching that of noninfected individuals of the same age. [64][65]
    • Individuals with HIV infection on adequate antiretroviral therapy are more likely to develop chronic comorbidities (e.g., cardiovascular disease, diabetes, cancer) than healthy individuals. [66][67]
  • Individual prognosis depends on various factors, including:
    • Adequate antiretroviral treatment
    • Viral set point; and CD4 count
    • Exposure to opportunistic pathogens
    • Individual genetic properties
    • HIV species and subtype
    • Preexisting conditions

Preventiontoggle arrow icon

Risk reduction [68]

All patients should be counseled on the following risk reduction measures.

HIV preexposure prophylaxis (PrEP) [69]

HIV postexposure prophylaxis (PEP) [73]

Special patient groupstoggle arrow icon

HIV in pregnancy

Intrapartum management of HIV [74][75]
Maternal viral load near time of delivery Delivery method Intrapartum antiretroviral treatment Infant prophylaxis
> 1000 copies/mL OR unknown viral load OR poor adherence to ARV treatment
> 50–≤ 1000 copies/mL
  • IV zidovudine is administered based on an individualized decision.
≤ 50 copies/mL
  • Postpartum management
    • Postexposure prophylaxis in neonates: See “Infant prophylaxis” in the table above.
    • Breastfeeding should generally be avoided in countries with good food availability and hygienic baby food (e.g., clean drinking water) , because risk of transmission is 5–20%.
    • See “Perinatally acquired HIV.”
  • Diagnosis in infants: : if < 18 months, diagnosis is confirmed via PCR, not ELISA

Suspect HIV in infants with failure to thrive, diffuse lymphadenopathy, diarrhea, and thrush, especially if the mother is a high-risk patient.

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