A Second Virus Responding to Its Vector To Initiate Transmission
While many pathogens actively contribute to their own transmission, viruses are widely held to be strictly passive. Transmission activation, i.e., a viral response to vectors on infected hosts regulating virus uptake and transmission, has been described for a single virus, cauliflower mosaic virus. Berthelot et al. (e01822-18) found that a second virus, turnip mosaic virus, actively contributes to its own transmission through transmission activation, suggesting that this might be a general transmission strategy.
H2O2 activates virus transmission.
Portal Protein: the Universal Nucleator of dsDNA Virus Assembly
The presence of a single portal ring is required to form infectious virions for many double-stranded DNA (dsDNA) viruses. How only one portal is selectively incorporated at a unique vertex is unclear, but often the portal protein acts as an assembly nucleator, ensuring its incorporation. Motwani and Teschke (e00187-19) found that a portal protein nucleates assembly of P22 procapsid-like particles. Addition of portal rings to an assembly reaction increases the rate of formation and yield of particles and corrects improper particle morphology. These data suggest that procapsid assembly universally initiates with a nucleation complex composed minimally of portal and scaffolding proteins.
Portal protein rings nucleate assembly of procapsid-like particles in vitro.
Antiviral NF-κB Signaling during Human Cytomegalovirus Infection
Human cytomegalovirus (HCMV) is a significant cause of morbidity in neonates and the immunosuppressed. HCMV extensively modulates NF-κB signaling during infection, yet how key NF-κB constituents contribute to HCMV infection has remained elusive. Goodwin and Munger (e02030-18) found that the two major NF-κB regulatory kinases, IKKα and IKKβ, limit the initiation of HCMV infection and attenuate viral replication and cell-to-cell transmission. These findings shed light on the HCMV–NF-κB pathogen-host interaction.
IKKα and IKKβ restrict wild-type HCMV infection.
Tissue-Resident CD4+ and CD8+ T Cells Protect against Recurrent Genital Herpes Infection
Reactivation of herpes simplex virus 2 (HSV-2) from latency causes viral shedding that can develop into recurrent genital lesions. Using phenotypic and functional immunological assays in a guinea pig model, Srivastava et al. (e02309-18) found that tissue-resident CD4+ and CD8+ T-cell-mediated mechanisms contribute to protection against recurrent genital herpes. These results provide insights into the immune mechanisms of HSV-2 recurrence and suggest candidate antigens for incorporation in future therapeutic mucosal vaccines.
Protection induced by RR2 associated with functional vaginal mucosa-resident CD8+ T cells.
Respiratory Syncytial Virus Infection Primes Mice for High Titers of Vaccine-Induced Neutralizing Antibodies
Humans may experience repeated infections caused by the same serotype of respiratory syncytial virus (RSV), in contrast to infections with most other viruses. The effects of any residual but nonprotective immunity on responses to RSV vaccines are not well understood. McGinnes Cullen et al. (e00087-19) found that a single injection of RSV prefusion F protein-containing virus-like particles (VLPs) stimulates high titers of neutralizing antibodies in animals previously infected with RSV, while a second RSV infection or postfusion F-containing VLPs does not. This result shows that a properly constructed immunogen can be an effective vaccine in animals previously infected with RSV.
RSV neutralizing antibody titers after VLP immunizations of mice previously infected with RSV.
- Copyright © 2019 American Society for Microbiology.
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- A Second Virus Responding to Its Vector To Initiate Transmission
- Portal Protein: the Universal Nucleator of dsDNA Virus Assembly
- Antiviral NF-κB Signaling during Human Cytomegalovirus Infection
- Tissue-Resident CD4+ and CD8+ T Cells Protect against Recurrent Genital Herpes Infection
- Respiratory Syncytial Virus Infection Primes Mice for High Titers of Vaccine-Induced Neutralizing Antibodies
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