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HIV targets the body’s immune system—specifically CD4 T cells. The virus is transmitted through bodily fluids but can remain undetected in its host for years, causing a diverse array of complications. During the progression of HIV infection, a patient’s CD4 lymphocyte count will decrease. Individuals with HIV who do not receive treatment can develop AIDS once their CD4 lymphocyte count decreases; these patients are highly susceptible to opportunistic infection. Patients that develop AIDS and remain untreated have a 1 to 2 years prognosis of survival.[1] Due to the loci of infection, managing the virus uses a multifaceted approach. The core of HIV treatment is highly active antiretroviral therapy (HAART). In most patients, HAART includes 2 nucleoside reverse transcriptase inhibitors (NRTIs) and an integrase strand transfer inhibitor (InSTI).[2] These regimens seek to interrupt viral replication and slow disease progression. Abacavir is an NRTI.[3] Abacavir causes a hypersensitive response in 5% to 8% of patients treated. Cytotoxic T cells mediate the hypersensitivity reaction to abacavir. Hypersensitivity reactions (HSR) can occur within the first 6 weeks of treatment if genetic prescreening is not conducted. If the drug is continued despite worsening symptoms, the severity of the HSR can escalate over time. Symptoms of an HSR typically include at least 2 of the following: fever, rash, fatigue, cough, difficulty breathing, and gastrointestinal issues such as nausea, vomiting, or abdominal pain.[4][5] If an HSR is suspected, abacavir should be discontinued immediately. Should the symptoms of a clinically diagnosed HSR improve after stopping abacavir, it is crucial to avoid reintroducing the drug, as this can lead to immediate and potentially life-threatening reactions, including anaphylaxis and death.[6] The signs and symptoms of abacavir hypersensitivity are nonspecific and may be confused with other conditions frequently encountered in HIV-positive patients, such as infections, immune restoration disease, and hypersensitivity reactions to other medications.[7] Therefore, understanding the mechanism and predictive power of the major histocompatibility complex, class I, B 57:01 (HLA-B*57:01) allele concerning hypersensitive reactions is critical in shaping the best clinical practices.[8]

Hypersensitivity can manifest as a variety of symptoms. The most common AHR symptoms include fever, chills, rash, gastrointestinal, and respiratory symptoms. Patch testing is often used to confirm hypersensitivity and will cause a palpable cutaneous response on the skin.[29]