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SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

Coronaviruses assemble by budding into the lumen of the endoplasmic reticulum-Golgi intermediate compartment. The viral E protein operates in this membrane morphogenetic process. Lopez et al. (p. 3000-3010) and Boscarino et al. (p. 2989-2999) demonstrate that coronavirus assembly functions depend on E protein posttranslational palmitoylation. The two studies provide new insights into the structures that drive assembly and release of enveloped virus particles.

Varicella-Zoster Virus Is a Structurally Crippled Herpesvirus

Varicella-zoster virus (VZV) is renowned for its low titer when grown in cultured cells. There remains no single explanation for this diminished infectivity. Carpenter et al. (p. 2821-2835) examined VZV particles using several imaging techniques and discovered that >75% were light particles (envelopes without capsids). Viral particles were observed at the base of filopodia on the cell surface. This abundance of aberrant coreless particles further emphasizes that the VZV assembly process is remarkably disordered and bears limited resemblance to that of the closely related herpes simplex virus.

A New Class of Influenza A Virus Particles

Influenza viruses are usually tested for infectivity by the capacity to infect eggs or form plaques. Ngunjiri et al. (p. 2673-2680) used a clonogenic assay to detect and quantify influenza A virus cell-killing particles (CKPs). Some virus populations were found to contain a large excess of CKPs that are not infectious. These noninfectious CKPs cause a delay in apoptosis and require functional polymerase to kill cells. Identification of noninfectious CKPs adds to the array of phenotypes found in influenza virus populations, each with the potential to regulate pathogenesis.

Triggering an Antiviral State in Human Dendritic Cells

Dendritic cells (DCs) play a central role in antiviral immune responses, but these cells also serve as viral targets. Kramer et al. (p. 2930-2937) provide evidence that viral RNA present in phagocytosed virus-infected cells induces an antiviral state in human DCs. This antiviral state is characterized by upregulation of viral sensors such as Mda-5 and RIG-I and effector molecules like PKR. Uptake of infected cells inhibits echovirus replication in DCs and prevents echovirus-induced cell death. These findings suggest a mechanism for protection of DCs in an environment with ongoing viral infection.

Failure of a Human Immunodeficiency Virus Type 1 Vaccine and Subsequent Immunity

The disappointing lack of efficacy of human immunodeficiency virus type 1 (HIV-1) vaccines tested thus far underscores the importance of better understanding the mechanisms of vaccine failure. Balamurugan et al. (p. 2784-2791) provide a detailed examination of a DNA gag vaccinee who became infected with HIV-1 and compare him to a coinfected individual who had not been vaccinated. The results demonstrate that failure of the vaccine did not reduce the capacity of the vaccinee to mount Gag-specific cytotoxic T-lymphocyte responses or apply immune pressure against HIV-1. This work suggests that vaccine failure does not have a deleterious effect on cellular immunity against HIV-1.

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