A study involving IRTA-CReSA reveals that plitidepsin can block the replication of viruses such as SARS-CoV-2, MERS-CoV, Zika, respiratory syncytial virus, and herpes, among others.
Currently, there are no effective treatments for many viruses, and in many cases, the only option is for the immune system to overcome the infection on its own. Now, research published in Nature Communications demonstrates that plitidepsin, an anti-cancer drug, can act as an antiviral against different viruses. The study, led by IrsiCaixa, included contributions from research teams at the Animal Health Research Center (IRTA-CReSA), the Josep Carreras Institute, and the pharmaceutical company PharmaMar.
IRTA-CReSA played a key role in this study by helping assess the antiviral efficacy of plitidepsin in experimental models. Our team conducted in vitro and in vivo tests to determine how this drug affects the replication of various viruses of interest for human health. These findings reinforce the idea that plitidepsin could be a promising candidate for developing new broad-spectrum antivirals.
According to Julia Vergara, a researcher at IRTA-CReSA, “Our studies, in collaboration with leading research centers in Catalonia and across Spain, have demonstrated that plitidepsin shows highly promising antiviral activity against viruses from diverse families. These results open new perspectives for developing innovative and broad-spectrum antiviral therapies.”
This study reveals that plitidepsin not only blocks its known therapeutic target but also modulates other molecular processes within cells, creating a unique "molecular footprint." This cellular modulation prevents many viruses from replicating, offering an innovative strategy for antiviral development.
Additionally, the research confirmed that plitidepsin regulates the production of inflammatory proteins such as IL-6, which could be key in treating diseases like long COVID, where chronic inflammation plays a significant role. Furthermore, initial clinical trials with hospitalized COVID-19 patients suggest that this drug can reduce the need for oxygen within two days.
Most antivirals today are designed to directly target viruses. However, due to the high mutation rate of these microorganisms, they can quickly develop resistance to existing treatments. For this reason, researchers propose studying other drugs with mechanisms similar to plitidepsin to create a portfolio of broad-spectrum antivirals capable of acting quickly against new viral threats.
Vergara also states, “The high mutation rate of viruses and the variability between different virus families can limit the effectiveness of current antivirals, which are primarily designed to target pathogens directly. That’s why it is essential to explore alternative strategies, like plitidepsin, to develop broad-spectrum antivirals that can respond quickly and effectively to new viral threats. Focusing on the host factors that viruses use to enter cells and replicate could be key to developing broad-spectrum drugs.”
