Rosmarinic acid inhibits Rift Valley fever virus: in vitro, computational and analytical studies

Author:

Farouk Faten1ORCID,Zarka Mohamed A2,Al-Sawahli Majid Mohammed34ORCID,Hassan Amr5,Mohamed Aly Fahmy6ORCID,Ibrahim Ibrahim M7ORCID,El-Rahman Mohammed Fafy Abd8ORCID,Shebl Rania Ibrahim9ORCID

Affiliation:

1. Pharmaceutical Chemistry Department, Faculty of Pharmacy, Ahram Canadian University (ACU), 6th October City, Giza, Egypt

2. Department of Pharmacognosy, College of Pharmacy, The Islamic University, Najaf, Iraq

3. Department of Pharmaceutics, College of Pharmacy, The Islamic University, Najaf, Iraq

4. Department of Pharmaceutical Technology, Faculty of Pharmacy, Kafr Elsheikh University, Kafr Elsheikh, Egypt

5. Department of Bioinformatics, Genetic Engineering & Biotechnology, Research Institute (GEBRI), University of Sadat City, Sadat, Egypt

6. The International Center for Training & Advanced Researches (ICTAR), Cairo, Egypt

7. Department of Biophysics, Faculty of Science, Cairo University, Cairo, Egypt

8. Botany Department, Faculty of Women for Arts, Science & Education, Ain Shams University, Cairo, Egypt

9. Department of Microbiology & Immunology, Faculty of Pharmacy, Ahram Canadian University (ACU), 6th October City, Giza, Egypt

Abstract

Aim: The antiviral potentials of rosmarinic acid (RA) against Rift Valley fever (RVF) virus were investigated. Methods: Antiviral activity was investigated by evaluating the reduction in the viral infectivity titer. Computational and LC–MS studies were performed for investigating the mechanism of action. This is via testing the interaction between RA and its major metabolite with the key infectivity proteins and determination of RA cellular permeability. Results: A superior reduction in RVF infectivity titer (45.5%) was observed when RA was applied post-infection compared to 17.7% reduction following its application before infection in addition to time-dependent inactivation kinetics. Recorded data showed in-silico inhibitory potential of RA and its metabolite against RVFV cap-binding protein and glycoprotein C, which are integral for viral transcription. LC–MS revealed cellular inclusion of RA, supporting its intracellular viral interaction. Conclusion: These antiviral potentials might suggest a promising foundation for future anti-RVF drug development.

Publisher

Future Medicine Ltd

Subject

Virology

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