Molecular Pathogens 2024, Vol.15, No.1, 9-16 http://microbescipublisher.com/index.php/mp 13 genetic material of HIV, RNA, undergoes frequent mutations and recombinations, leading to the emergence of a wide range of subtypes and variant strains within the virus population. This variability enables the virus to evade attack by the host immune system, including antibody recognition and binding (Teresa et al., 2019). Antibodies recognize antigens on the surface of pathogens through their specific structure, with variable regions that have specific amino acid sequences capable of binding to specific areas on the surface of the pathogen. However, due to the variability of HIV, the antigenic epitopes on the surface of the virus can undergo changes, leading to mutations or the disappearance of regions that were previously bound by antibodies. These changes in antigenic epitopes can render antibodies unable to recognize and bind to the virus as the antigenic targets have been altered. This variability can occur in surface proteins of the virus (such as the Env protein of HIV) or other key proteins that play a critical role in the binding process of antibodies. The variability of HIV also leads to the emergence of multiple subtypes and variant strains with distinct epitope and structural characteristics. This makes it challenging for a single antibody to cover all subtypes and variant strains as antibodies can only bind to specific antigens. Therefore, an antibody may have strong binding capacity for one subtype or variant strain but may be ineffective against other subtypes or variant strains. 4 The Consequences of Antibody Escape Mutation and Viral Infection 4.1 The definition and mechanism of antibody escape mutation Antibody escape mutation refers to the ability of HIV, due to its high degree of variability and high replication rate, to produce mutations that allow the virus to evade attack by the host immune system's antibodies during infection. This mutation enables the virus to avoid antibody recognition and binding, thereby protecting itself from immune system attacks (Liu et al., 2019). The mechanisms of antibody escape mutation mainly include point mutations and structural changes. Point mutations refer to changes in individual nucleotides in the viral genome, leading to changes in the antigenic epitopes recognized by antibodies. These mutations may alter the structure, charge, or affinity of epitopes, making it difficult for antibodies to effectively bind. The virus can also weaken or prevent antibody binding by changing the amino acid sequence surrounding the antibody binding site (Montoya et al., 2018). Structural changes refer to the structural modifications of epitopes through mechanisms such as deletion, insertion, or rearrangement during infection. These changes can alter the structure and affinity of antibodies for the virus, making antibodies lose their specificity for the epitopes recognized by the original antibodies. Antibody escape mutation plays a crucial role in HIV transmission and viral replication. This mutation allows the virus to evade host immune system surveillance, establish persistent infection in hosts, and lead to further virus transmission and development. Given the antigenic variability of HIV, developing broad-spectrum antibody-based drugs and vaccines that target different subtypes and variant strains remains a challenge. 4.2 The impact of antibody escape mutation on viral infection Due to the high degree of virus variability and the existence of escape mechanisms, antibody escape mutation enables the virus to effectively evade the host immune system's antibody attack, thereby increasing the persistence and replicative capacity of the virus infection. Antibody escape mutation allows the virus to avoid being quickly cleared by antibodies. When the virus enters the host, the immune system produces specific antibodies to recognize and bind to virus particles, thereby neutralizing or marking the virus for clearance by the host immune system. However, HIV has developed new antigenic epitopes through mutation, avoiding specific antibody binding and making it difficult for the host immune system to effectively clear the infection. This allows the virus to persist and replicate within the host. Antibody escape mutation also leads to the development of drug resistance in the virus. During antiviral treatment, selective pressure can guide the virus to develop drug-resistant mutations, making previously sensitive antiviral
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