HIV needs specific receptors to enter CD4+ T cells. The main ones are CCR5 and CXCR4. The most common mutation associated with resistance is CCR5-delta32. People with this homozygous mutation lack functional CCR5 receptors, which is a co-receptor for many HIV strains, especially R5 tropic viruses. So, if the virus can't enter the cells, it can't replicate, leading to undetectable levels and preserved CD4 counts.
The options likely include CCR5, CXCR4, maybe others like CCR3 or CXCR3. The correct answer is CCR5. The other receptors are either used by different HIV strains or not involved in entry. CXCR4 is for X4 viruses, which usually appear later in disease. CCR3 and CXCR3 aren't typically involved in HIV entry. So the answer is CCR5.
**Core Concept**
HIV requires specific chemokine co-receptors (e.g., CCR5, CXCR4) to enter CD4+ T cells. Genetic mutations in these co-receptors can confer resistance to HIV infection or progression.
**Why the Correct Answer is Right**
The **CCR5 receptor** is the primary co-receptor for most HIV strains (R5-tropic viruses). A homozygous mutation (e.g., CCR5-Δ32) leads to a nonfunctional receptor, preventing viral entry. This explains the patient’s undetectable viral load and preserved CD4 count despite HIV positivity. The absence of functional CCR5 disrupts the R5-tropic HIV entry pathway, effectively halting replication.
**Why Each Wrong Option is Incorrect**
**Option A:** CXCR4 is used by X4-tropic HIV strains, which typically emerge in late-stage disease. It is not the primary entry route for initial infection.
**Option C:** CCR3 is not a known HIV co-receptor.
**Option D:** CXCR3 is involved in Th1 immune responses but not HIV entry.
**Clinical Pearl / High-Yield Fact**
**CCR5-Δ32 homozygosity** is the most well-known genetic resistance mechanism to HIV. Patients with this mutation are "elite controllers" and rarely progress to AIDS. This discovery underpins CCR5 antagonist therapies (e.g., maraviroc) used in HIV treatment.
**Correct Answer: C. CCR5**
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