eMedicine Specialties > Infectious Diseases > HIV

Early Symptomatic HIV Infection

Robert J Carpenter, DO, Fellow in Infectious Diseases, Infectious Diseases Clinic, Naval Medical Center San Diego
Braden R Hale, MD, MPH, Assistant Clinical Professor, Department of Internal Medicine, University of California at San Diego; Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Naval Medical Center at San Diego; Kirk M Chan-Tack, MD, Fellow, Division of Infectious Disease, University of Maryland School of Medicine; John Bartlett, MD, Chief of Division of Infectious Diseases, Chief of HIV Care Service, Professor, Department of Internal Medicine, Johns Hopkins University School of Medicine

Updated: Jun 9, 2009

Introduction

Background

The clinical effects of human immunodeficiency virus (HIV) infection are diverse, ranging from an acute retroviral syndrome associated with primary HIV infection to a prolonged asymptomatic state to advanced HIV disease. Experts regard HIV disease as beginning at the time of primary (acute) HIV infection and progressing through numerous stages of chronic infection.

Acute HIV infection is defined as the period between exposure to the virus and completion of the initial immune responses. This period varies but generally lasts 2-3 months. During this time, the antibody test may be negative for HIV, but the serum viral load (the amount of HIV virus in the blood) is detectable and can be quite high (millions of copies per milliliter).

In most infected individuals, active virus replication and progressive immunologic impairment occur throughout the course of HIV infection, even during the clinically latent stage. Chronic HIV disease can be divided empirically based on the degree of immunodeficiency into (1) early stage (ie, CD4 T-cell count >500/µL), (2) intermediate stage (ie, CD4 T-cell count 200-500/µL), and (3) advanced stage (ie, CD4 T-cell count <200/µL).

Approximately 70% of patients with HIV infection develop symptoms during the acute infection period,¹ although some reports of symptomatic acute HIV infection are likely associated with a reporting bias, and the actual frequency may be lower. Symptoms associated with HIV seroconversion are nonspecific and may be attributed to a viral syndrome such as influenza virus infection.

Complex changes occur in the immune system during the acute infection period, including rapid depletion of CD4 cells. Anti-HIV antibodies are produced, and cytotoxic CD8 lymphocytes destroy HIV-infected cells. Unfortunately, the response is imperfect, and latent reservoirs of HIV infection are established throughout the body.

Chronic HIV infection begins after antibodies to the virus have fully developed and the initial immune response is complete. HIV disease with active virus replication usually progresses during this asymptomatic period, and the rate of disease progression correlates directly with HIV RNA levels. Individuals with high levels of HIV RNA progress to symptomatic HIV disease faster than patients with low levels of HIV RNA. Some individuals develop symptoms or organ dysfunction during chronic infection due to direct effects of the virus rather than a defect in cell-mediated immunity. Some infected persons who are otherwise asymptomatic develop persistent generalized lymphadenopathy (PGL) during this time. With few exceptions, CD4 cell counts decline progressively during this asymptomatic period, at an average rate of approximately 50 cells/µL/y.

Acquired immunodeficiency syndrome (AIDS) is the condition that results from long-term (chronic) HIV infection and is defined by an absolute CD4 cell count of less than 200 cells/µL and specific opportunistic infections or malignancies. The interval between acute HIV infection and AIDS is highly variable, with a median time of approximately 10 years. In many infected individuals, an opportunistic disease is the first manifestation of HIV infection. When the CD4 cell count falls to below approximately 200 cells/µL, the resulting state of immunodeficiency places the individual at high risk for opportunistic infections and neoplasms (clinically apparent HIV disease).

Pathophysiology

Acute HIV infection (also known as seroconversion) is defined as the period between exposure to the virus and completion of the initial immune responses (when an antibody test becomes positive for HIV). After infection, HIV is able to replicate at an exponential rate using CD4 cells. The following is a simplified outline of events that occur during acute HIV infection:²

Day 0: The individual is exposed to HIV, and infection begins.
Day 8: The virus is detectable in blood using polymerase chain reaction (PCR); however, antibody test findings are negative. The amount of virus in the blood more than doubles every day. The CD4 cell count (and total WBC count) begins to drop as the viral load increases.
Week 2-4: Early antibodies to HIV may be detected; however, they have a low affinity for viral antigens and have little effect on the virus itself. Newer antibody assays may detect these antibodies. The viral load peaks and begins to decline as the immune system begins to battle the virus with antibodies and CD8 cytotoxic cells. (Although persons infected with HIV may transmit the infection to another person at any time, they are highly infectious during the period of acute infection when genital shedding of HIV virus peaks [at approximately week 3-4 of acute infection]. Because the individual may be asymptomatic during this period, he or she may have no knowledge that he or she is infected and may therefore not be using appropriate safer-sex precautions. This represents an epidemiologic challenge in controlling the HIV pandemic.)
Week 10-24: The HIV viral load drops to its lowest point, also known as the set point, which is different in each person. Antibodies now have higher affinity for viral antigen; therefore, antibody tests become positive for HIV. Seroconversion is now complete, and chronic HIV infection begins.

Frequency

United States

In 2006, a study of people requesting HIV testing at a sexually-transmitted diseases (STD) clinic in San Francisco found 136 new HIV infections of 3,789 people tested. Eight percent of those with HIV infection were acutely infected (antibody findings negative, antigen findings positive). This study found that acute HIV infections were associated with having a known HIV-positive partner within the past 12 months and a history of hepatitis B, syphilis, and chlamydia infection in the past 2 years.³
A larger, prospective study of 109,250 people seeking HIV testing in North Carolina found 606 new HIV infections, 4% of which were acute infections (antibody findings negative, antigen findings positive). Seventy percent of the acute HIV infections were in people who were tested at STD clinics.⁴
Clearly, the prevalence of acute HIV infection varies and depends on geography, as well as demographics of the population tested.

Mortality/Morbidity

Acute HIV infection has a range of presentations. Morbidity varies depending on the condition. Mortality associated with acute HIV infection is uncommon.

Race

Early symptomatic HIV infection has no reported racial predilection.

Sex

Both sexes are affected with the constellation of symptoms that define the syndrome of acute HIV infection.

Age

Early symptomatic HIV infection can affect individuals of any age.

Clinical

History

Acute human immunodeficiency virus (HIV) infection manifests as numerous signs and symptoms and can affect multiple systems. The most common presentations include asymptomatic infection, fever, chills, malaise, fatigue, swollen lymph nodes, sore throat, and myalgias.²

Approximately 30% of individuals with acute HIV infection are asymptomatic but are highly infectious; this represents an epidemiologic challenge in controlling the HIV pandemic.
Constitutional: Patients with acute HIV infection may experience fever, chills, malaise or fatigue, night sweats, anorexia, and weight loss.
Lymphatics: Swollen lymph nodes are common, especially in the groin, head, and neck.
Nose and throat: Patients may experience sore throat, with or without ulcers or thrush.
Gastrointestinal: Nausea, emesis, diarrhea, and transaminitis may develop.
Musculoskeletal: Joints may be asymmetrically swollen and tender; myalgias are also common.
Neurologic: Personality changes, headache, and painful or stiff neck can be seen during acute HIV infection.

Physical

Physical findings of acute HIV infection are nonspecific and may mimic those of other viral infections, such as influenza virus infection. In addition, many of these findings resolve without medical intervention. The most common findings include fever and chills, lymphadenopathy, pharyngitis, anemia, thrombocytopenia, and rash.

Fever and chills
Lymphadenopathy: During the examination, the nodes are generally discrete and freely mobile and may be tender.
Oral lesions
- Pharyngitis is a common finding.
- Thrush manifests as a white exudate, often with an erythematous mucosa. Thrush develops most commonly on the soft palate. Early lesions can also be found along the gingival border. The diagnosis is made based on clinical appearance or direct examination of a scraping for pseudohyphal elements, which are characteristic of candidiasis (typically with Candida albicans). Severe cases of thrush can involve the esophagus, with resultant dysphagia or odynophagia.
- Oral hairy leukoplakia manifests as filamentous white lesions, generally along the lateral borders of the tongue.
- Herpes simplex virus (HSV) causes lesions. Oral and genital lesions are most common, but perianal and periungual lesions are also observed. Herpetic lesions resemble a cluster of vesicles on an erythematous base.
- Reactivation of herpes zoster (shingles) is characterized by lesions due to varicella-zoster virus (VZV) that may extend over several dermatomes. Widespread cutaneous dissemination may occur, but visceral involvement has not been reported.
- Aphthous ulcers are shallow and painful and usually affect the posterior oropharynx.
Hematologic
- Anemia may be present, and the physical examination may reveal pallor.
- In thrombocytopenia associated with acute HIV infection, as in other forms of thrombocytopenia, bleeding is rare, unless the platelet count falls to below 10,000 cells/µL. If this occurs, bleeding gums, extremity petechiae, and easy bruising are common presentations.
Dermatologic: Rash may develop and is usually maculopapular, primarily on the trunk and/or proximal extremities.
Neurologic
- Aseptic meningitis may manifest as headache, photophobia, and frank encephalitis. Cranial nerve involvement may be observed. Cranial nerve VII is affected predominantly; sometimes, nerves V and/or VIII are also affected.
- Findings of acute inflammatory demyelinating polyneuropathy include weakness, areflexia, and minimal sensory changes.
- Patients with mononeuritis multiplex develop multifocal asymmetric cranial or peripheral nerve lesions, including facial or laryngeal palsy, wristdrop or footdrop, and other neuropathic symptoms. Early in the course of HIV infection, mononeuritis multiplex is usually limited to a single nerve or a few nerves and resolves spontaneously without treatment.
- Myopathy is characterized by proximal muscle weakness as the primary clinical finding.
- Encephalopathy or encephalitis can also be seen in acute HIV infection.

Causes

Persistent generalized lymphadenopathy: This is often the earliest symptom of HIV infection after primary infection. Because of marked follicular hyperplasia in response to HIV infection, the lymph nodes have very high viral concentrations. Persistent generalized lymphadenopathy may be observed at any point in the spectrum of immune dysfunction and is not associated with an increased likelihood of developing AIDS.
Oral lesions
- Thrush: This can result from Candida infection and oral hairy leukoplakia, presumably due to Epstein-Barr virus (EBV) infection. Thrush is usually a sign of fairly advanced immunologic decline, generally occurring in individuals with CD4 cell counts of 200-500 cells/µL.
- HSV lesions: The finding of HSV lesions can also reflect deteriorating immune function in patients infected with HIV.
- Aphthous ulcers of the posterior oropharynx: These affect 10-20% of patients infected with HIV. Their etiology is unknown. These ulcers can be very painful and can cause dysphagia if left untreated.
Hematologic
- Anemia
  - All other causes of anemia should be excluded systematically before concluding that anemia is due to HIV infection.
  - Upon disease progression, individuals with HIV infection develop a moderate-to-severe hypoproliferative anemia.
  - The most common form of anemia observed in patients infected with HIV has the characteristics of anemia of chronic disease.
  - Anemia may be a complication of opportunistic infections and/or may be due to marrow damage from the virus or from drug toxicity (eg, zidovudine, also known as azidothymidine [AZT]).
- Thrombocytopenia
  - Thrombocytopenia may also be an early manifestation of HIV infection. Approximately 3% of patients infected with HIV with CD4 cell counts greater than 400 cells/µL have platelet counts of less than 150,000 cells/µL. Of patients who have CD4 cell counts less than 400 cells/µL, 10% also have platelet counts of less than 150,000 cells/µL.
  - HIV-associated thrombocytopenia is rarely a serious clinical problem. In most cases, platelet counts remain greater than 50,000 cells/µL and the condition can be treated conservatively.
  - Idiopathic thrombocytopenia in persons with HIV infection is very similar to the thrombocytopenia observed in individuals with idiopathic thrombocytopenic purpura (ITP). Antibodies against HIV (anti-GP160/120) have been shown to also bind to platelets (anti-GPIIb/IIIa).⁵ Because these data point to an immunologic basis for thrombocytopenia in persons infected with HIV, most of the treatments used are immune-based.
  - Another mechanism for HIV-induced thrombocytopenia is a direct effect of HIV on megakaryocytes, evidenced by a defect and subsequent decrease in platelet production.
  - In patients infected with HIV, thrombocytopenia has also been reported as a consequence of classic thrombotic thrombocytopenic purpura (TTP). This clinical syndrome, consisting of fever, thrombocytopenia, hemolytic anemia, and neurologic and renal dysfunction, is a rare complication of early HIV infection.
Neurologic
- Aseptic meningitis: This can be observed in all but the very late stages of HIV infection. This suggests that aseptic meningitis in the setting of HIV infection is an immune-mediated disease. Aseptic meningitis due to HIV infection usually resolves spontaneously within 2-4 weeks. Signs and symptoms may persist long-term in some patients.
- Acute inflammatory demyelinating polyneuropathy: Through unknown mechanisms, HIV infection can mimic Guillain-Barré syndrome.
- Mononeuritis multiplex: A necrotizing arteritis of peripheral nerves, mononeuritis multiplex is another autoimmune peripheral neuropathy observed in patients infected with HIV.
- Myopathy: AZT can cause myopathy; this is often reversible once the drug is discontinued. HIV infection can also cause myopathy by direct damage to the muscle cells. The exact mechanism has not yet been elucidated.
Dermatologic: Reactivation of herpes zoster (shingles): Observed in 10-20% of patients infected with HIV infection, shingles indicates a modest decline in immune function and is often the first clinical indication of immunodeficiency.

Differential Diagnoses

Workup

Laboratory Studies

Patients with suspected acute human immunodeficiency virus (HIV) infection should undergo serum testing for HIV antibody and HIV antigen using HIV nucleic acid amplification, HIV p24 antigen, or PCR for viral load. Beware of false-positive HIV viral load test results (<15,000 RNA copies/mL blood).^6,4
Persistent generalized lymphadenopathy: This is diagnosed clinically. Lymph node biopsy is not indicated in patients with early-stage HIV disease unless the patient has signs and symptoms of systemic illness (eg, fever, weight loss) or enlarged, fixed, or coalescent lymph nodes. A serologic diagnosis of acute EBV or CMV mononucleosis should be considered.
Thrush: This is diagnosed based on clinical appearance or examination of a scraping for pseudohyphal elements. Culturing is of no value because throat cultures are positive for Candida in most patients with HIV infection, even those without thrush. See Thrush for more details.
Oral hairy leukoplakia: This is typically diagnosed based on clinical appearance. Biopsy tissue findings reveal epithelial hyperplasia with protruding hairs and minimal inflammation. EBV can be visualized with electron microscopy, immunofluorescence, or Southern blot analysis. See Hairy Leukoplakia for more details.
Aphthous ulcers: These are diagnosed clinically. Examination of biopsy tissue reveals nonspecific inflammation and is not diagnostic. The primary role for biopsy is when aphthous ulcers are difficult to distinguish from HSV lesions. See Aphthous Stomatitis for more details.
Herpes simplex virus: Viral culture is the criterion standard for diagnosis. Viral PCR of intralesional fluid is also highly sensitive. Direct fluorescent antigen (DFA) is also a useful and generally rapidly available test that yields good sensitivity and specificity. Tzanck preparation (ie, Giemsa stain of vesicle contents) may reveal multinucleated giant cells and intranuclear inclusions specific for HSV or VZV, but the sensitivity is low. See Herpes Simplex for more details.
Varicella-zoster virus: Viral culture is the criterion standard for diagnosis. DFA is also a useful and generally rapidly available test with good sensitivity and specificity. Results from a Tzanck preparation (ie, Giemsa stain of vesicle contents) may reveal multinucleated giant cells and intranuclear inclusions specific for HSV or VZV, but the sensitivity is low. See Herpes Zoster for more details.
Anemia: A thorough evaluation is essential to exclude all other causes of anemia, especially any correctable causes. In addition to the workup detailed in Anemia, measuring the serum erythropoietin (EPO) level can help distinguish between bone marrow damage (ie, normal EPO level) and inflammatory anemia (ie, low EPO level).
Thrombocytopenia: A thorough evaluation is essential to exclude all other causes of thrombocytopenia (eg, see Thrombotic Thrombocytopenic Purpura), such as drug toxicity, lymphoma, fungal infection, and mycobacterial infection. Bone marrow examination generally reveals a normal or increased number of megakaryocytes.
Elevated transaminases: Acute viral hepatitis A, B, and C should be excluded with appropriate serologic testing.
Neurologic: A lumbar puncture is an important element of the evaluation in patients with HIV infection who have neurologic abnormalities. A lumbar puncture is most helpful in the diagnosis of opportunistic infections.
- Aseptic meningitis or encephalitis: Cerebrospinal fluid examination reveals lymphocytic pleocytosis, an elevated protein level, and a normal glucose level.
- Acute inflammatory demyelinating polyneuropathy: Cerebrospinal fluid examination reveals pleocytosis and increased protein levels. A peripheral nerve biopsy reveals findings of a perivascular infiltrate, suggesting an autoimmune etiology. Electromyography (EMG) findings reveal demyelination.
- Myopathy: Serial creatine kinase levels are useful for monitoring the course of HIV myopathy. EMG is a sensitive diagnostic test in patients with HIV myopathy. The most common finding after muscle biopsy is scattered myofiber degeneration with occasional inflammatory infiltrates. Other pathological findings include nemaline rod bodies, cytoplasmic bodies, and mitochondrial abnormalities.

Other Tests

Electromyography
- The finding in acute inflammatory demyelinating polyneuropathy is demyelination.
- EMG is also useful for evaluating mononeuritis multiplex; results generally reveal multifocal axonal neuropathy.
- EMG is a sensitive test for the evaluation of HIV myopathy.

Procedures

Acute inflammatory demyelinating polyneuropathy - Peripheral nerve biopsy
Mononeuritis multiplex - Nerve biopsy
Myopathy - Muscle biopsy
Meningitis/encephalitis - Lumbar puncture and CSF analysis

Histologic Findings

Thrush: Microscopic examination of a lesion scraping shows pseudohyphal elements.
Oral hairy leukoplakia: Biopsy tissue reveals epithelial hyperplasia with protruding hairs and minimal inflammation. EBV can be visualized with electron microscopy, immunofluorescence, or Southern blot analysis.
HSV and VZV: Tzanck preparation (ie, Giemsa stain of vesicle contents) may reveal multinucleated giant cells and intranuclear inclusions specific for HSV or VZV.
Thrombocytopenia: Bone marrow examination generally reveals a normal or increased number of megakaryocytes.
Acute inflammatory demyelinating polyneuropathy: Peripheral nerve biopsy reveals a perivascular infiltrate suggestive of an autoimmune etiology.
Mononeuritis multiplex: Biopsy of nerve tissue reveals inflammation and vasculitis. In some cases, CMV inclusions have been found.
Myopathy: The most common muscle biopsy finding is scattered myofiber degeneration with occasional inflammatory infiltrates. Other pathological findings include nemaline rod bodies, cytoplasmic bodies, and mitochondrial abnormalities.

Treatment

Medical Care

Antiretroviral treatment of acute human immunodeficiency virus (HIV) infection is controversial. However, treating acute HIV infection has several theoretical advantages, as follows:¹

To treat some symptomatic patients
To halt viral evolution at a time of minimal viral diversity, prior to viral adaptations to specific host immune responses
To protect developing immune responses from the deleterious effects of sustained HIV viremia
To reduce the viral set-point
To limit the latent pool of infection

Several studies have shown no benefit for short-term combination antiretroviral therapy during acute infection.⁷ However, a 2006 retrospective study found that an initiation of combination therapy within 2 weeks of HIV seroconversion was associated with sustained viral load and CD4 cell count benefits for up to 72 weeks after termination of therapy.⁸ In 2007, another group found that the CD4 cell count decline over 3 years was slower after cessation of 3 months of antiretroviral therapy started during acute infection when compared with those who did not receive acute therapy.⁹ CD4 counts appear to deplete very rapidly during acute HIV infection. Thus, treatment to prevent early loss of cells may be impractical in most circumstances.

In 2008, a subset analysis of the Strategic Management of Antiretroviral Therapy (SMART) study found that initiation of combined antiretroviral therapy at higher CD4 counts (>350 cells/µL) was associated with decreased morbidity and mortality in HIV disease.¹⁰

Evidence from the NIH Comprehensive International Program of Research on AIDS (CIPRA) HT 001 clinical study showed that starting antiretroviral therapy at CD4⁺ T-cell counts between 200-350 cells/µL improves survival compared with deferring treatment until the CD4⁺ T-cell count drops to less than 200 cells/µL (the current standard of care). CIPRA HT 001 is a randomized, controlled, open-label clinical trial that was conducted in a resource-limited setting where the standard of care to initiate therapy was when CD4⁺ T cells were less than 200 cells/µL or when the patient had a clinical diagnosis of AIDS.¹¹

HIV-infected adults (n=816) with early HIV disease were randomly assigned to either begin antiretroviral therapy within 2 weeks of enrollment or when they were diagnosed with clinical AIDS or when their CD4⁺ T-cell count fell to below 200 cells/µL. Six participants in the early treatment group had died, while 23 participants in the standard-of-care group had died. Also, among participants who began the study without tuberculosis infection, 18 individuals in the early treatment group developed tuberculosis, while 36 people in the standard-of-care group developed tuberculosis. These interim results were statistically significant and led to ending the trial early to offer antiretroviral therapy to all participants in the standard-of-care group with a CD4⁺ T-cell count of less than 350 cells/µL.

Given the heterogeneity of medical evidence regarding treatment of acute HIV infection, the current Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents, published by US Department of Health and Human Services, consider treatment of acute infection optional and recommend enrollment in a clinical trial.

Surgical Care

Idiopathic thrombocytopenic purpura: Splenectomy is an option in patients whose conditions are refractory to medical treatment. Most patients with HIV-associated thrombocytopenia respond to this surgical treatment. Because of the risk of infections with encapsulated organisms, all patients infected with HIV, especially those who are about to undergo splenectomy, must be immunized with pneumococcal polysaccharide vaccine.
Thrombotic thrombocytopenic purpura: Splenectomy is also an option in refractory cases of TTP, but the response rate is highly variable. Because of the risk of infections with encapsulated organisms, all patients infected with HIV, especially those who are about to undergo splenectomy, must be immunized with pneumococcal polysaccharide vaccine.

Consultations

Close collaboration with consultants (eg, infectious diseases specialists, dermatologists, gastroenterologists, hematologists, neurologists) is important and is directed by the constellation of HIV manifestations.

Medication

Many drugs are used to treat human immunodeficiency virus (HIV) infection, and new drugs are in development. See the article HIV Disease in eMedicine’s Infectious Diseases volume for a discussion of current treatment options. The most up-to-date list of FDA-approved drugs can be found at AIDSinfo Drug Database.

Follow-up

Further Inpatient Care

Most of the conditions involved in early symptomatic human immunodeficiency virus (HIV) infection can be treated in an outpatient setting. Decisions for inpatient care are made on a case-by-case basis. Patients infected with HIV should be cared for by providers with expertise in HIV infection because this has been shown to decrease patient morbidity and to extend patient lifespan.

Inpatient & Outpatient Medications

See Medication.

Prognosis

Early symptomatic HIV infection encompasses several diseases. Patients classified under this term are a heterogeneous group, with widely varying clinical problems and prognoses. Generally, HIV infection carries an excellent prognosis in most patients who are cared for by a provider who is experienced in HIV medicine.

Patient Education

Counsel patients extensively about the course of HIV illness, therapeutic options, health maintenance issues (eg, immunizations, abstinence, safer-sex practices, informing sexual partners about HIV diagnosis), and the range of conditions that can occur at each stage on the HIV continuum. Close follow-up care with providers who have expertise in treating patients infected with HIV is essential.
For excellent patient education resources, visit eMedicine's Immune System Center, Sexually Transmitted Diseases Center, and Teeth and Mouth Center. Also, see eMedicine's patient education articles HIV/AIDS, Rapid Oral HIV Test, Oral Herpes, and Canker Sores.

Miscellaneous

Medicolegal Pitfalls

Failure to identify patients who are at risk for human immunodeficiency virus (HIV) infection: One of the goals of this article is to remind clinicians that the numerous conditions discussed may be harbingers of HIV infection. A high index of clinical awareness is essential. A growing body of literature supports routine testing for HIV.

References

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Truong HM, Grant RM, McFarland W, Kellogg T, Kent C, Louie B. Routine surveillance for the detection of acute and recent HIV infections and transmission of antiretroviral resistance. AIDS. Nov 14 2006;20(17):2193-7. [Medline].
Pilcher CD, Fiscus SA, Nguyen TQ, Foust E, Wolf L, Williams D. Detection of acute infections during HIV testing in North Carolina. N Engl J Med. May 5 2005;352(18):1873-83. [Medline].
Bettaieb A, Fromont P, Louache F, et al. Presence of cross-reactive antibody between human immunodeficiency virus (HIV) and platelet glycoproteins in HIV-related immune thrombocytopenic purpura. Blood. Jul 1 1992;80(1):162-9. [Medline].
Mylonakis E, Paliou M, Lally M, et al. Laboratory testing for infection with the human immunodeficiency virus: established and novel approaches. Am J Med. Nov 2000;109(7):568-76. [Medline].
Streeck H, Jessen H, Alter G, Teigen N, Waring MT, Jessen A. Immunological and virological impact of highly active antiretroviral therapy initiated during acute HIV-1 infection. J Infect Dis. Sep 15 2006;194(6):734-9. [Medline].
Hecht FM, Wang L, Collier A, Little S, Markowitz M, Margolick J. A multicenter observational study of the potential benefits of initiating combination antiretroviral therapy during acute HIV infection. J Infect Dis. Sep 15 2006;194(6):725-33. [Medline].
Fidler S, Fox J, Touloumi G, Pantazis N, Porter K, Babiker A. Slower CD4 cell decline following cessation of a 3 month course of HAART in primary HIV infection: findings from an observational cohort. AIDS. Jun 19 2007;21(10):1283-91. [Medline].
Strategies for Management of Antiretroviral Therapy (SMART) Study Group, Emery S, Neuhaus JA, Phillips AN, Babiker A, Cohen CJ, et al. Major clinical outcomes in antiretroviral therapy (ART)-naive participants and in those not receiving ART at baseline in the SMART study. J Infect Dis. Apr 15 2008;197(8):1133-44. [Medline].
US Department of Health and Human Services. National Institutes of Health. NIH News. Starting Antiretroviral Therapy Earlier Yields Better Clinical Outcomes. June 8, 2009. [Full Text].
Aberg JA, Gallant JE, Anderson J, et al. Primary care guidelines for the management of persons infected with human immunodeficiency virus: recommendations of the HIV Medicine Association of the Infectious Diseases Society of America. Clin Infect Dis. Sep 1 2004;39(5):609-29. [Medline].

Keywords

early symptomatic HIV infection, acute HIV infection, acute retroviral syndrome, HIV seroconversion illness, HIV seroconversion syndrome, immune reconstitution inflammatory syndrome, human immunodeficiency virus, HIV, viral infection, immunologic impairment, immunocompromise, pre-acquired immune deficiency syndrome, pre-AIDS, thrush, oral hairy leukoplakia, herpes simplex virus, HSV, varicella-zoster virus, VZV, shingles, herpes zoster, thrombocytopenia, acute inflammatory demyelinating polyneuropathy, mononeuritis multiplex, myopathy, persistent generalized lymphadenopathy, PGL, oral lesions, anemia, aseptic meningitis, aphthous ulcers

Contributor Information and Disclosures

Author

Robert J Carpenter, DO, Fellow in Infectious Diseases, Infectious Diseases Clinic, Naval Medical Center San Diego
Robert J Carpenter, DO is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Osteopathic Association, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Braden R Hale, MD, MPH, Assistant Clinical Professor, Department of Internal Medicine, University of California at San Diego; Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Naval Medical Center at San Diego
Braden R Hale, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Kirk M Chan-Tack, MD, Fellow, Division of Infectious Disease, University of Maryland School of Medicine
Kirk M Chan-Tack, MD is a member of the following medical societies: American College of Physicians, American Medical Association, Christian Medical & Dental Society, Physicians for Social Responsibility, and Southern Medical Association
Disclosure: Nothing to disclose.

John Bartlett, MD, Chief of Division of Infectious Diseases, Chief of HIV Care Service, Professor, Department of Internal Medicine, Johns Hopkins University School of Medicine
John Bartlett, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Clinical Pharmacology, American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, American Thoracic Society, American Venereal Disease Association, Association of American Physicians, Infectious Diseases Society of America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

Fred A Lopez, MD, Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine
Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Speaking and teaching

Further Reading