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Host cells permissive to dengue virus (DENV) infection are primarily defined by their expression of specific surface receptors that facilitate viral attachment and entry. These include myeloid lineage cells such as monocytes, macrophages, and dendritic cells, which utilize receptors like DC-SIGN (CD209) and the mannose receptor to internalize the virus (PMID: 22440960, Nature Reviews Microbiology, 2013). Additionally, hepatocytes and endothelial cells are susceptible, contributing to the systemic nature of the infection and complications like plasma leakage. The permissivity of these cells is central to DENV pathogenesis, as they serve as the primary sites for viral replication and the subsequent "cytokine storm" associated with severe dengue (NIH, 2022). Therapeutic interventions targeting host cell permissivity include entry inhibitors and host-directed antivirals that disrupt the replication cycle within these specific cell populations (PMID: 28533540). However, the phenomenon of antibody-dependent enhancement (ADE) remains a significant challenge, as it can increase the number of infected permissive cells and exacerbate disease severity (PubMed, 2021).
Inhibition of viral entry, alpha-glucosidase inhibition, or modulation of host lipid metabolism to prevent viral assembly and release (PMID: 28533540).
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