1. Literature Cited Li, X., Kukkonen, S., Vapalahti, O., Plyusnin, A., Lankinen, H., and Vaheri, A. 2004. Tula Hantavirus Infection of Vero E6 Cells Induces Apoptosis Involving Caspase 8 Activation. Journal of General Virology 85:3261- 3268. Hepojoki, J., Strandin, T., Lankinen, H., and Vaheri, V. 2012. Hantavirus Structure- Molecular Interactions Behind the Scene. Journal of General Virology 93:1631-1644. Ogoina, D. 2011. Fever, fever patterns and diseases called ‘fever’- A review. Journal of Infection and Public Health: 4:3:108-124. Leclerq, I., Batejat, C., Burguiere, A., and Manuguerra, J. 2014. Heat Inactivation of the Middle East Respiratory Syndrome Coronavirus. Life Science Weekly: 2906.. The Effects of Temperature on Hantavirus Glycoproteins and their Ability to Infect Vero E6 Cells Introduction  Hantaviruses which include Hantaan Virus (HTNV), Puumala Virus (PUUV), and Andes Virus (ANDV) are part of the larger Bunyaviridae family. They usually infect rodents, which exhibit increased aggression. However, if humans are infected hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome result (Li et al. 2004).  All Hantaviruses are made up of small, medium, and large RNA segments. The medium segment is what encodes for the glycoproteins on the outside of the virus, Gn and Gc. These two glycoproteins are involved in receptor binding and membrane fusion. (Hepojoki et al. 2012).  Fevers can be brought on by viral infections, which causes a decrease in the growth rate of the virus. The classification of fevers is based upon duration or temperature of fever. The height of a fever has only been shown to loosely correlate to the severity of the illness. (Ogoina 2011).  Enveloped viruses like influenza have shown to be completely inactivated at 56°C (Leclerq et al. 2014). There is no known connection between variation in temperature and structure of viral glycoproteins.  It is known that fever plays a role in the growth rate of viruses after infection, but little is known about the role of elevated body temperature and viral entry.  A pseudovirus system was used in order to ensure only one viral entry per virus. Pseudoviruses have a VSV core with a Renilla luciferase gene. The Gn and Gc glycoproteins normally expressed on each virus are on the outside of the pseudovirus. Hypothesis  The increase in incubation temperature from 37°C to 39°C will decrease the infection rates of all three pseudoviruses. Acknowledgements I would like to thank Dr. Higa for her support throughout this project and Dr. Kaltreider for his help with the cell proliferation assay part of the project. Emily Skutnik* and Dr. Meda Higa Department of Biological Sciences, York College of Pennsylvania Culture Vero E6 Cells Complete Titration to Determine Relative Infection Rates of VSV, HTNV, PUUV, and ANDV at different dilutions using Renilla luciferase assay Culture Vero E6 Cells Infect Vero E6 Cells with VSV, HTNV, PUUM, and ANDV using viral dilutions based on titration results and incubate for 24 hours at 37˚C and 39˚C Add DMEM (10%FBS) media to Vero E6 Cells and incubate for 24 hours at 37˚C and 39˚C Measure viral infection rates using Renilla luciferase assay Measure cell viability using non- radioactive cell proliferation assay Methods Results Conclusions  Increased viral infection was observed at 37°C compared to 39°C even though cell viability was higher at 39°C for the control group.  Differences in glycoproteins on the outside of pseudoviruses dictate how well they are able to invade host cells. http://www.icjournal.org/ArticleImage/1086IC/ic-41-323-g002-l.jpg VSV rLuc L M S HTNV Gn Gc RNA Polymerase Gn Gc http://wwwnc.cdc.gov/eid/images/03-0458-F1.jpg