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The Measles virus (MeV) is a highly infectious, enveloped, single-stranded RNA virus that targets the host immune system to facilitate its replication and systemic spread. It enters host cells primarily through the Signaling Lymphocytic Activation Molecule (SLAMF1/CD150) on immune cells and Nectin-4 on respiratory epithelial cells (Tatsuo et al., 2000; Muhlebach et al., 2011). A defining feature of MeV infection is the induction of "immune amnesia," characterized by the depletion of pre-existing memory T and B lymphocytes, which significantly increases susceptibility to opportunistic pathogens for months or years following recovery (Mina et al., 2015; Petrova et al., 2019). The virus also produces non-structural proteins, such as the V and C proteins, which inhibit the host's innate immune response by blocking interferon signaling (PubMed). While there are no FDA-approved small-molecule antivirals specifically for measles, Vitamin A is the standard of care to reduce morbidity, and the live-attenuated MMR vaccine provides long-term immunity (WHO). Understanding the MeV-host interaction is critical for managing outbreaks and developing potential antiviral therapies targeting viral entry or replication machinery.
Vitamin A acts as an immunomodulator and maintains epithelial integrity to reduce measles-related morbidity (WHO). Ribavirin acts as a guanosine analog to inhibit viral RNA-dependent RNA polymerase, though its use is typically off-label for severe cases (PubMed). Vaccines induce neutralizing antibodies against the Hemagglutinin (H) and Fusion (F) surface glycoproteins to prevent viral entry (CDC).
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