Molecular and Cellular Virology

To date, the available therapeutic arsenal remains restricted to a limited number of viral diseases. The efficacy of treatments for infections such as hepatitis C or HIV/AIDS relies on combination therapies targeting distinct molecular pathways, thereby minimizing the risk of resistance development. Among emerging viral threats, several coronaviruses and the hepatitis E virus (HEV) are classified as high-risk pathogens for zoonotic spillover events. However, therapeutic interventions against the diseases they induce remain severely limited. HEV represents the most common etiologic agent of acute hepatitis globally, with an estimated 100 million infections annually. Epidemiological data attribute 14 million symptomatic cases and 300,000 deaths to HEV each year. Historically, HEV was primarily associated with waterborne outbreaks in low- and middle-income countries, driven by inadequate sanitation infrastructure. Recent evidence, however, confirms its endemic and zoonotic circulation in high-income settings, including Europe. As a result, HEV has emerged as the leading cause of acute hepatitis in several developed countries, including France. The Coronaviridae family has long been recognized as a reservoir for emerging pathogens, a hypothesis corroborated by the recent emergence of SARS-CoV-2. Phylogenetic and epidemiological analyses strongly suggest that future coronavirus outbreaks are not only probable but inevitable, given the persistent zoonotic interface and viral adaptability.

Our laboratory is developing multiple complementary strategies to combat these viral pathogens. At the fundamental level, we focus on dissecting the viral life cycle within host cells, a critical step for identifying novel therapeutic targets. The intracellular cycle of these viruses is organized into four key stages:

1. Viral entry, enabling delivery of the viral genome into the host cell;
2. Viral replication, during which the viral genome is amplified;
3. Viral morphogenesis, leading to the assembly of new virions;
4. Secretion of newly formed virions, completing the cycle.

Our team’s primary objective is to elucidate how these viruses hijack the host cellular machinery to complete their replicative cycle. This mechanistic understanding is essential for uncovering vulnerabilities that can be targeted therapeutically.

In parallel, we employ high-throughput screening of chemical libraries and plant extracts to identify potential antiviral compounds. The mechanisms of action of these compounds are then characterized in detail, providing insights into both their therapeutic potential and the viral processes they disrupt.

By integrating these two approaches—fundamental mechanistic studies of the viral cycle and targeted antiviral discovery—we establish a comprehensive framework that advances both therapeutic innovation and fundamental knowledge of viral replication.