Anita Meier

For years I've been wondering why I see DNA blobs in the cytosol of HSV-1 infected cells! A new study shows that HSV-1 infections trigger the shedding of nuclear DNA into the cytoplasm possibly through cellular mechanosensing. This blebbing might activate IFN signaling through cGAS.

Our latest paper is out! 🎉 We show that the HSV-1 origin binding protein UL9 tethers dsDNA thereby forming intramolecular DNA loops and intermolecular DNA tethers. 🤝 www.nature.com/articles/s41...

We also show that UL9-induced loops form rapidly and don't migrate or change size. This indicates tethering of two sites rather than loop extrusion.

Our latest paper is out! 🎉 We show that the HSV-1 origin binding protein UL9 tethers dsDNA thereby forming intramolecular DNA loops and intermolecular DNA tethers. 🤝 www.nature.com/articles/s41...

However, using force spectroscopy we found that UL9 very efficiently (~55%) introduces large (~300bp) loops in larger DNA templates independent of the origin sequence. ATP binding but not hydrolysis destabilises those loops.

Our latest paper is out! 🎉 We show that the HSV-1 origin binding protein UL9 tethers dsDNA thereby forming intramolecular DNA loops and intermolecular DNA tethers. 🤝 www.nature.com/articles/s41...

Rotavirus (RV) is the leading cause of severe childhood diarrhea. To enter the host cell, RV must first activate its spike protein. This occurs when trypsin, a digestive enzyme found in the intestine, cleaves specific regions of the spike protein. Hence, ensuring tissue specificity.

Herpes simplex virus type 1 (HSV-1) tightly packages its DNA within the capsid and creates a pressure of ~20 atm that is used to inject the genome into the cell nucleus. Check out this beautiful structure of the capsid and portal vertex:

Herpes simplex virus type 1 (HSV-1) tightly packages its DNA within the capsid and creates a pressure of ~20 atm that is used to inject the genome into the cell nucleus. Check out this beautiful structure of the capsid and portal vertex:

We partially originate from viruses! This week I found out that part of the mitochondrial replication machinery (polymerase and helicase-primase) has its ancestry in bacteriophages. 🤯

Most viruses rely on the host to provide the entire translation machinery. However, giant viruses have evolved to encode part of the machinery themselves. Latest discovery: mimivirus (APMV) encodes its own initiation factor (vIF4F) and specifically promotes translation of viral mRNA!

Studying viruses helps us understand cellular processes: the breakthrough discovery of RNA splicing in 1977 was achieved by studying adenovirus (AdV) biology. They used mRNA/ DNA hybridization and electron microscopy.

Some of the weirdest viruses: Multipartite viruses have segmented genomes that are enclosed in different capsids, which are independently transmitted. All segments have to meet in the same host cell for complementation. The evolutionary benefit for this lifestyle is unclear.

Zika virus induces nanotube formation 👾 in the host cell to facilitate viral spread. ZIKV even uses them to acquire mitochondria from neighbouring uninfected cells!

Epstein-Barr virus encodes a protein called EBNA1, which physically tethers 🤝 the viral DNA to the host chromosome so it doesn't get lost during mitosis. www.cell.com/cell/fulltex...

Herpes simplex virus type 1 (HSV-1) infections dramatically change the architecture of the host nucleus. HSV-1 specifically recruits certain host factors (e.g. RNAPII) to promote its replication. HSV-1 actively rewires the human genome! 😲Look at how the host genome gets squeezed!!

This is a tupanvirus, ~450nm in diameter ~1.2um in length, clearly one of the giant viruses. It encodes for the most complete translational machinery found in viruses with only the ribosome lacking. Most (non-giant) viruses don't encode any components required for translation. It's so fluffy!! 😱

Blows my mind 🤯 that it is possible to capture the structural dynamics of viral capsid contraction by thawing and re-freezing the ice within the electron microscope! Anyone interested in microsecond time-resolved cryo-EM should check out this paper: www.nature.com/articles/s41...

Weird virus fact: Papillomaviruses can make their host cell immortal 🧟‍♂️ by activating telomerase (together with other mechanisms). The viral protein E6 regulates and directly interacts with hTERT and telomeric DNA.

Weird virus fact: Papillomaviruses can make their host cell immortal 🧟‍♂️ by activating telomerase (together with other mechanisms). The viral protein E6 regulates and directly interacts with hTERT and telomeric DNA.

Weird virus fact: HIV-1 and other retroviruses hijack cellular tRNA and use it as primer to initiate reverse transcription of their RNA genome. They exploit the same tRNA terminal 3′-OH group used by the host for aminoacylation and peptidyl transfer.

pmc.ncbi.nlm.nih.gov/articles/PMC...