宿主的遗传构成影响对病毒感染的不同反应。人群对逆转录病毒的抵抗研究由于无法进行原理性研究而变得复杂。纯系小鼠的表型易感性范围广，是鉴定和描述抵抗机制及其遗传基础的理想工具。YBR/Ei小鼠感染一个黏膜传播的乳腺肿瘤病毒，但将病毒从其谱系中消除。病毒消除与易感小鼠中阻断抗病毒反应的主要机制之一，即病毒特异性新生儿口服耐受态有关。病毒控制与病毒中和抗体、细胞毒性CD8+T细胞、NK细胞和NK T细胞无关，后者是抵抗逆转录病毒最为典型机制。我们鉴定了一个控制抵抗机制的单个显性位点，暂时命名为“病毒滴度衰减位点(Avt)”，并将其定位于第18号染色体的远端区域。重要性 阐明介导逆转录病毒抵抗机制的方式对于人类健康至关重要，因为这最终将揭示个体在对微生物感染易感性方面的遗传差异知识。

Differential responses to viral infections are influenced by the genetic makeup of the host. Studies of resistance to retroviruses in human populations are complicated due to the inability to conduct proof-of-principle studies. Inbred mouse lines, which have a range of susceptible phenotypes to retroviruses, are an ideal tool to identify and characterize mechanisms of resistance and define their genetic underpinnings. YBR/Ei mice become infected with Mouse Mammary Tumor Virus, a mucosally transmitted murine retrovirus, but eliminate the virus from their pedigrees. Virus elimination correlates with a lack of virus-specific neonatal oral tolerance, which is a major mechanism for blocking the anti-virus response in susceptible mice. Virus control is unrelated to virus-neutralizing antibodies, cytotoxic CD8+ T cells, NK cells, and NK T cells, which are the best characterized mechanisms of resistance to retroviruses. We identified a single, dominant locus that controls the resistance mechanism, which we provisionally named attenuation of virus titers (Avt) and mapped to the distal region of chromosome 18. IMPORTANCE Elucidation of the mechanism that mediates resistance to retroviruses is of fundamental importance to human health, as it will ultimately lead to knowledge of the genetic differences among individuals in susceptibility to microbial infections.