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  Human immunodeficiency virus (HIV) is a blood-borne and sexually transmitted infection that leads to acquired immunodeficiency syndrome (AIDS).

  
  
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  HIV belongs to the Lentivirus genus of the retroviridae family.

  
  
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  An enveloped, single-stranded RNA virus that primarily infects CD4+ T lymphocytes (though it can infect other cell that express CD4, such as macrophages).

  
  
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  Viral life cycle

  
  
  
  
  1. 
     

     Infection of the host cell via binding to CD4 and fusion of the viral envelope and cell membrane.

     
     
  2. 
     

     The viral RNA is reverse transcribed in DNA and integrated into the host genome.

     
     
  3. 
     

     There is a period of latency, followed by an active viral replication phase.

     
     
  4. 
     

     New viral particles “bud off” of the cell membrane of the infected cell.

     
     
  5. 
     

     This eventually results in cellular destruction and consequently impairment of the host’s immune system.

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  HIV can spread via blood, semen, vaginal fluid, or breast milk.

  
  
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  Primary HIV infection can be asymptomatic or present as a viral prodrome occurring 2 to 4 weeks after exposure.

  
  
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  Symptoms include fever, reactive cervical lymphadenopathy, pharyngitis, maculopapular rash, orogenital ulcers, and meningoencephalitis.

  
  
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  Leukopenia and decreased CD4 count can also occur with associated opportunistic infections.

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  HIV is diagnosed via anti-HIV antibodies detected in serum. These are persistently present 3 months following exposure.

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  Takes into account the myriad of clinical manifestations associated with HIV infection (Appendices A and B).

  
  
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  Useful for establishing baseline, assessing the effect of therapy, monitoring long term follow-up, and prognosticating.

  
  
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  Immune status (as measured by CD4 count) is useful in clinical decision making.

  
  
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  The likelihood of developing clinical manifestations of immunodeficiency has been shown to correlate with decreasing CD4 count.

  
  
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  Normal absolute CD4 count in adults is 500 to 1500 cells per mm³ of blood (normal values require age-adjustment, as children generally have higher CD4 counts than adults). Opportunistic infections and other manifestations of HIV become more likely when CD4 counts drop below 200 cells/mm³.

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  Incorporates both clinical manifestations and CD4 count. It was initially designed for surveillance purposes, though it provides an adequate overview of a patient’s clinical picture (Table 11-1).

  
  
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  Classified into one of five stages (0, 1, 2, 3, unknown) as follows:

  
  
  
  
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    Stage 0—HIV-positive patient, with a previous negative HIV test within 6 months of seroconversion. These patients remain Stage 0 until 6 months after diagnosis.

    
    
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    Stage 1—Acute HIV infection. Occurs within 2 to 4 weeks after HIV infection. Symptoms may include flu-like illness.

    
    
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    Stage 2—Clinical latency (HIV inactivity or dormancy). Asymptomatic or chronic HIV infection.

    
    
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    Stage 3—AIDS. Presence of AIDS-defining condition = Stage 3.

    
    
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    Stage unknown—No information available on CD4 count and no information available on AIDS-defining conditions.

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  Consists primarily of medications that target specific viral enzymes and comprises a treatment regimen known as antiretroviral therapy (ART). This has previously been termed highly active antiretroviral therapy (HAART) and subsequently combined ART (cART), though all three are synonymous.

  
  
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  Five classes of drugs and treatment consist of a cocktail of three or four agents.

  
  
  
  
  1. 
     

     Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)

     
     
  2. 
     

     Nonnucleoside reverse transcriptase inhibitors (NNRTIs)

     
     
  3. 
     

     Protease inhibitors (PI)

     
     
  4. 
     

     Entry inhibitors (EIs)

     
     
  5. 
     

     Integrase inhibitors

  
  
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  ART is initiated immediately upon diagnosis, regardless of CD4 count. Previously, ART was initiated only after CD4 count fell below a threshold of 350 cell/mm³ or AIDS-defining illness was present. However, two large randomized controlled trials (ART-START and TEMPRANO) demonstrated approximately 50% reduction in morbidity and mortality among patients who started ART immediately after diagnosis.

  
  
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  Pre-exposure prophylaxis (PrEP)

  
  
  
  
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    Truvada (emtricitabine/tenofovir disoproxil)

    
    
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    For high-risk individuals, and reduces the risk of transmission of HIV via sexual activity by 90% and via intravenous drug use by 70%

  
  
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  Post-exposure prophylaxis (PEP)

  
  
  
  
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    Reduces the risk of seroconversion after potential exposure to HIV

    
    
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    Must be initiated within 72 hours after potential exposure, and ideally within 1 hour of exposure

    
    
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    Consists of three antiretroviral medications taken for 4 week’s duration

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  Approximately 36.7 million individuals living with HIV worldwide, in 2016.

  
  
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  Up to 50% of immunosuppressed patients present with head and neck complaints. HIV and immunodeficiency may present in the salivary gland, aerodigestive tract, sinonasal cavity, temporal bone, or cervical lymph nodes.

  
  
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  The head and neck manifestations of HIV are present in four general categories of diseases:

  
  
  
  
  1. 
     

     Infectious/inflammatory conditions as a result of immunodeficiency

     
     
  2. 
     

     Complicated infection as a result of immunodeficiency

     
     
  3. 
     

     Malignancy related to immunodeficiency

     
     
  4. 
     

     AIDS-related illness

Salivary Gland

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  HIV may affect any of the salivary glands, but the parotid gland is the most common due to the presence of intraparotid lymph nodes.

  
  
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  Salivary gland lesions are particularly prevalent in the pediatric population, representing up to 18% of the primary complaints that yield a diagnosis of HIV.

  
  
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  The initial evaluation of the parotid gland should include a thorough history and head and neck physical examination.

  
  
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  Parotid lesions are generally infectious, inflammatory, or neoplastic in nature.

  
  
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  Parotid neoplasms can be further grouped as follows:

  
  
  
  
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     Primary lesions of the salivary gland itself (benign or malignant)

     
     
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     Primary tumors arising from the parotid lymph nodes

     
     
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     Metastatic tumors to the parotid lymph nodes

  
  
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  Specific differential diagnoses need consideration in the evaluation of the HIV-positive patient. Benign lymphoepithelial cysts (BLECs) and diffuse infiltrative lymphocytosis are common benign etiologies of the salivary gland. When malignancy is suspected, the common malignancies seen in HIV-positive patients must be considered, particularly Kaposi sarcoma, lymphoma, and metastatic cutaneous malignancies.

  
  
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  Diagnosis can be confirmed via fine needle aspiration in the majority of cases.

  
  
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  Diagnostic imaging with ultrasound, CT, or MRI is useful when clinically indicated.

  
  
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  Approximately 75% of parotid lesions are BLECs. About 6% represent neoplasms and the remainder consists of infectious/inflammatory processes.

Benign Lymphoepithelial Cyst

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  The most common parotid gland lesions seen in HIV-positive patients.

  
  
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  Etiology is related to viral inflammation.

  
  
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  May present as unilateral lesions but imaging often reveals subclinical disease bilaterally. BLECs are bilateral in up to 80% of cases.

  
  
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  Typically present asymptomatically, though compression of the parotid ducts from the cysts can cause pain and sialadenitis.

  
  
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  Cervical lymphadenopathy is present in up to 90% of cases.

  
  
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  BLEC may be confused for papillary cystadenoma lymphomatosum (Warthin tumor)—both are cystic and bilateral.

Management

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  No definitive surgical excision is required for BLEC.

  
  
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  Treatment goals consist of decreasing the viral load with use of ART, which causes regression of the cysts.

  
  
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  Options include the following (complete response rates of nonsurgical therapy, based on a recent meta-analysis):

  
  
  
  
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     ART (52.8%)

     
     
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     Serial aspiration for cosmesis (33.3%)

     
     
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     Sclerotherapy with doxycycline injections has also been described (55.5%)

     
     
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     High-dose external beam radiotherapy (65.8%)

     
     
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     Parotidectomy is typically reserved for large, disfiguring lesions or if malignancy is suspected.

Diffuse Infiltrative Lymphocytosis Syndrome

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  Clinically similar to Sjogren syndrome seen in HIV-positive patients.

  
  
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  Incidence is approximately 1% of HIV patients.

  
  
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  Clinical presentation: Diffuse parotid enlargement and sicca symptoms (ie, xerostomia and xerophthalmia).

  
  
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  Associated with interstitial lymphocytic pneumonitis in 50% of cases.

  
  
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  Histologically, diffuse infiltrative lymphocytosis syndrome is characterized by lymphocytic infiltration with CD8 lymphocytes (vs CD4 in Sjogren syndrome).

Management

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  Primarily symptom control with salivary substitutes and sialogogues.

  
  
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  As with other causes of xerostomia, dental caries are a potential complication and referral to dentistry is warranted.