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Review demonstrates HIV relies on cellular signaling and complex stability for replication, suggesting novel antiviral interventions.
Calcium (Ca²⁺) homeostasis is essential for cellular signaling and protein trafficking. Viruses are comparatively simple organisms that leverage the availability of host cellular mechanisms for viral replication, including the manipulation of cellular Ca²⁺ dynamics-related processes. We review the dependence of HIV on cellular Ca²⁺ to promote viral replication, including stabilization of viral protein complexes in clinically latent HIV infected cells. We also discuss some of the general reliance of cellular Ca²⁺ homeostasis on viral propagation across several viruses. We discuss viral manipulations of cellular Ca²⁺ regulation for viral replication, specifically for viral assembly, complex stability, and disassembly. We close with an exploration of therapeutic opportunities via Ca²⁺ homeostasis disruption to mediate dysregulation of viral complex formation for viral peptide antigen presentation. Thereby, we aim to unlock a novel strategy to achieve an antiviral effect by modulating host-cell regulatory processes.
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Brémaud et al. (2025) studied this question.
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