Medizinische Hochschule Hannover, Germany
Student: Manutea Serrero, Ph.D. fellow
Supervisor: Prof. Beate Sodeik
Unlike other acute viral infections, an infection with Herpes Simplex Virus type 1 (HSV-1) is not cleared even when the blisters have vanished from the lips. Like other alphaherpesviruses, HSV-1 establishes residence in neurons of the peripheral nervous system where it remains silent and hides from the immune system. The latent genomes in the neurons can be reactivated and induce the production of virus and cause the re-emergence of the blisters. In 2012, the WHO estimated that approximately half of the world population is infected with HSV-1 and that more than every tenth human carries HSV-2. While the immune system can usually control the infection, unfortunately immuno-compromised patients can develop life-threatening infections.
After entering a cell by fusion with a host membrane, HSV-1 injects its capsids containing the viral genomes into the cytosol where it recruits host proteins for transport along the intracellular microtubule transport system and migrates to the nuclear pores to release the viral genomes for transcription and replication into the nucleoplasm. Interestingly, immune cells such as macrophages or dendritic cells are much less susceptible to infection that epithelial cells, fibroblasts and neurons.
The purpose of this project is to investigate how HSV1 infection differs in specific cell types and to characterize cytosolic proteins that interact with the capsids during infection. For this purpose, our team has developed an experimental model that allows us to mimic steps of the infection and enables us to study interactions of capsids of different viral protein composition with cytosolic host factors. Ultimately, our aim is to determine whether these interacting host proteins could be targeted to block viral replication and to enable the development of novel therapeutic approaches.
Beate Sodeik, Professor
Institute of Virology
Hannover Medical School