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The Paramyxoviridae family consists of enveloped, negative-strand RNA viruses that cause a wide range of human and animal diseases, including measles, mumps, parainfluenza, and respiratory syncytial virus (RSV) infections [1][7]. These viruses are characterized by a lipid envelope containing two primary surface glycoproteins: an attachment protein (variously termed H, G, or HN) that binds to host cell receptors and a fusion (F) protein that mediates the merging of viral and host membranes [1][16]. Within the host cell, the viral genome is replicated and transcribed by a virus-encoded RNA-dependent RNA polymerase (RdRp) complex, consisting of the large (L) and phosphoprotein (P) subunits [2][12]. Therapeutic interventions against these pathogens primarily target the F protein using monoclonal antibodies to prevent entry, or target the L protein using nucleoside analogs and allosteric inhibitors to halt viral replication [3][4]. While vaccines are effective for some members like measles and mumps, others like RSV and parainfluenza lack broad vaccines, necessitating the development of potent antivirals [10][14]. Drug resistance through viral mutations and the challenge of achieving broad-spectrum activity across diverse genera remain significant hurdles in the clinical management of paramyxovirus infections [12][15].
Viral fusion inhibition; Inhibition of viral RNA-dependent RNA polymerase (RdRp); Neutralization of viral attachment glycoproteins; Allosteric inhibition of the polymerase complex; Inhibition of nucleocapsid (N) protein assembly.
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