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Reviews of "MX2 Restricts HIV-1 and Herpes Simplex Virus Type 1 by Forming Cytoplasmic Biomolecular Condensates that Mimic Nuclear Pore Complexes"

Reviewers: S R Jennings (Drexel University) | 📘📘📘📘📘 • C Sheppard & A Rasmussen (Imperial College London) | 📒📒📒◻️◻️ • P Stäheli & S Weigang (IUniversity of Freiburg) | 📘📘📘📘📘

Published onMay 08, 2024
Reviews of "MX2 Restricts HIV-1 and Herpes Simplex Virus Type 1 by Forming Cytoplasmic Biomolecular Condensates that Mimic Nuclear Pore Complexes"
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MX2 restricts HIV-1 and herpes simplex virus type 1 by forming cytoplasmic biomolecular condensates that mimic nuclear pore complexes
MX2 restricts HIV-1 and herpes simplex virus type 1 by forming cytoplasmic biomolecular condensates that mimic nuclear pore complexes
Description

Summary Human myxovirus resistance 2 (MX2) can potently restrict HIV-1 and herpesviruses at a post-entry step by a process that requires MX2 interaction with the capsids of these viruses. The involvement of other host cell factors in this process, however, remains poorly understood. Here, we mapped the proximity interactome of MX2 revealing strong enrichment of phenylalanine-glycine (FG)-rich proteins related to the nuclear pore complex as well as proteins that are part of cytoplasmic ribonucleoprotein granules. MX2 interacted with these proteins to form multiprotein cytoplasmic biomolecular condensates that were essential for its anti-HIV-1 and -herpes simplex virus-1 (HSV-1) activity. MX2 condensate formation required the disordered N-terminal region of MX2 and its dimerization. Incoming HIV-1 and HSV-1 capsids associated with MX2 at these dynamic cytoplasmic biomolecular condensates. Our results demonstrate that MX2 forms cytoplasmic condensates that act as nuclear pore decoys, which trap capsids and induce premature viral genome release, and thereby interfere with nuclear targeting of HIV-1 and HSV-1.

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Summary of Reviews: Reviewers found the study compelling, clearly demonstrating the mechanism by which MX2 forms cytoplasmic condensates with host factors to trap viral capsids and prevent proper nuclear targeting by HIV-1 and HSV-1. They commended the thorough experimental plan and found the conclusions to be well supported by the results shown. However, reviewers suggested further characterization of the role of certain accessory proteins due to inconsistent gene knockdown levels and expanding the discussion by comparing it with other similar anti-viral molecules like MX1 to better contextualize the findings.

Reviewer 1 (Stephen J…) | 📘📘📘📘📘

Reviewer 2 (Carol S… & Amalie R…) | 📒📒📒 ◻️◻️

Reviewer 3 (Peter S… & Sebastian W…) | 📘📘📘📘📘

RR:C19 Strength of Evidence Scale Key

📕 ◻️◻️◻️◻️ = Misleading

📙📙 ◻️◻️◻️ = Not Informative

📒📒📒 ◻️◻️ = Potentially Informative

📗📗📗📗◻️ = Reliable

📘📘📘📘📘 = Strong

To read the reviews, click the links below. 

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