
The comparison of the DPP4 (dipeptidyl peptidase 4) SARS-CoV-2 hypothesis to a cockroach likely stems from its persistence in scientific discussions, despite challenges or contradictory findings. Like a cockroach, which is notoriously difficult to eradicate, this hypothesis has continued to be debated, re-examined, and adjusted even as other theories regarding SARS-CoV-2 infection mechanisms gained prominence.
Early in the COVID-19 pandemic, there was speculation that DPP4, a receptor implicated in MERS-CoV infections, might also play a role in SARS-CoV-2 entry into cells. Since both MERS and SARS-CoV-2 are coronaviruses, it seemed plausible that DPP4 might be involved in SARS-CoV-2 infection as well. Although it was later found that ACE2 (Angiotensin-Converting Enzyme 2) is the primary receptor for SARS-CoV-2, the DPP4 hypothesis lingered. Studies continued to investigate whether DPP4 had a secondary role or whether patients on DPP4 inhibitors (commonly used in diabetes treatment) had different outcomes in COVID-19 cases. Even after evidence showed that DPP4 is not the primary receptor for SARS-CoV-2, the hypothesis persisted, with researchers looking at indirect mechanisms, such as DPP4’s role in immune modulation and inflammation, which might affect COVID-19 progression.
Some studies suggested that DPP4 inhibitors might impact the immune response in patients with severe COVID-19, leading to speculation that DPP4 could still have a role in disease severity, especially in patients with diabetes or cardiovascular conditions. Despite extensive research, evidence for the direct involvement of DPP4 in SARS-CoV-2 infection remains inconclusive or mixed. Yet, like a cockroach, the theory refuses to die. Researchers continue to explore niche roles for DPP4, whether as a potential therapeutic target or in understanding comorbidities like diabetes and their impact on COVID-19 outcomes.
In a recent publication, Eleftheriou et al. proposed that inhibitors of dipeptidyl peptidase‐4 (DPP‐4) are functional inhibitors of the main protease (Mpro) of SARS‐CoV‐2 [1]. Their predictions prompted the authors to suggest linagliptin, a DPP‐4 inhibitor and approved anti‐diabetes drug, as a repurposed drug candidate against the ongoing COVID‐19 pandemic. We used an enzymatic assay measuring the inhibition of Mpro catalytic activity in the presence of four different commercially available gliptins (linagliptin, sitagliptin, alogliptin and saxagliptin) and several structural analogues of linagliptin to study the binding of DPP‐4 inhibitors to Mpro and their functional activity. We show here that DPP‐4 inhibitors like linagliptin, other gliptins and structural analogues are inactive against Mpro.
The resilience of the DPP4 hypothesis also reflects the nature of scientific inquiry. Even when a hypothesis doesn’t fully pan out, aspects of it might still offer insights into disease mechanisms or therapeutic strategies. In the case of SARS-CoV-2, the ongoing investigation into DPP4 demonstrates the search for broader understanding, particularly in complex disease interactions.
References


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