Off the beaten track: Understudied microbes and their potential.

The world of microbes is diverse, but the majority of these fascinating organisms are not as famous (or perhaps infamous) as their pathogenic counterparts. Cell highlights six scientists whose work addresses some of the most fundamental questions in biology, even though their microbial models may seem a tad bit unconventional.

Curriculum Guidelines for Graduate and Undergraduate Virology Courses.

Curriculum guidelines for virology are needed to best guide student learning due to the continuous and ever-increasing volume of virology information, the need to ensure that undergraduate and graduate students have a foundational understanding of key virology concepts, and the importance in being able to communicate that understanding to both other virologists and nonvirologists. Such guidelines, developed by virology educators and the American Society for Virology Education and Career Development Committee, are described herein.

Components of the LINC and NPC complexes coordinately target and translocate a virus into the nucleus to promote infection.

Nuclear entry represents the final and decisive infection step for most DNA viruses, although how this is accomplished by some viruses is unclear. Polyomavirus SV40 transports from the cell surface through the endosome, the endoplasmic reticulum, and the cytosol from where it enters the nucleus to cause infection. Here we elucidate the nuclear entry mechanism of SV40.

Using virtual interviewing to create a more accessible hybrid academic job market.

Virtual interviewing has become ubiquitous with the academic job market. Here, we highlight the best practices for candidates and departments to consider when using virtual interviewing. We propose how virtual interviews can be leveraged and adapted for hybrid academic job searches combining virtual and in-person activities in a post-pandemic world.

mSphere of Influence: Viruses-Pathogens or Expert Cell Biologists?

Chelsey C. Spriggs works in the field of DNA viral entry with a specific interest in virus-host interactions. In this mSphere of Influence article, she reflects on how two papers, "The HCMV assembly compartment is a dynamic Golgi-derived MTOC that controls nuclear rotation and virus spread" (D.

Golgi-associated BICD adaptors couple ER membrane penetration and disassembly of a viral cargo.

During entry, viruses must navigate through the host endomembrane system, penetrate cellular membranes, and undergo capsid disassembly to reach an intracellular destination that supports infection. How these events are coordinated is unclear. Here, we reveal an unexpected function of a cellular motor adaptor that coordinates virus membrane penetration and disassembly.

How non-enveloped viruses hijack host machineries to cause infection.

Viruses must navigate the complex endomembranous network of the host cell to cause infection. In the case of a non-enveloped virus that lacks a surrounding lipid bilayer, endocytic uptake from the plasma membrane is not sufficient to cause infection. Instead, the virus must travel within organelle membranes to reach a specific cellular destination that supports exposure or arrival of the virus to the cytosol.

Expression of HPV-induced DNA Damage Repair Factors Correlates With CIN Progression.

Human papillomaviruses (HPVs) are DNA viruses with epithelial tropism. High-risk types of HPV are the causative agents of the majority of cervical cancers and are responsible for a number of other anogenital as well as oropharyngeal cancers. The life cycle of HPV is closely linked to the differentiation state of its host cell and is dependent on the activation of specific pathways of the DNA damage response.

Dynein Engages and Disassembles Cytosol-Localized Simian Virus 40 To Promote Infection.

During entry, polyomavirus (PyV) is endocytosed and sorts to the endoplasmic reticulum (ER), where it penetrates the ER membrane to reach the cytosol. From the cytosol, the virus moves to the nucleus to cause infection. How PyV is transported from the cytosol into the nucleus, a crucial infection step, is unclear.

Human Papillomavirus and the DNA Damage Response: Exploiting Host Repair Pathways for Viral Replication.

High-risk human papillomaviruses (HPVs) are the causative agents of cervical and other genital cancers. In addition, HPV infections are associated with the development of many oropharyngeal cancers. HPVs activate and repress a number of host cellular pathways to promote their viral life cycles, including those of the DNA damage response.

FANCD2 Binds Human Papillomavirus Genomes and Associates with a Distinct Set of DNA Repair Proteins to Regulate Viral Replication.

The life cycle of human papillomavirus (HPV) is dependent on the differentiation state of its host cell. HPV genomes are maintained as low-copy episomes in basal epithelial cells and amplified to thousands of copies per cell in differentiated layers. Replication of high-risk HPVs requires the activation of the ataxia telangiectasia-mutated (ATM) and ATM and Rad3-related (ATR) DNA repair pathways.