Scientists Identify Bat Coronavirus Capable of Entering Human Cells

An international team of researchers has identified a bat coronavirus that can bind to a human cell receptor, raising important questions about zoonotic spillover potential. The virus, found in the heart-nosed bat (Cardioderma cor) in East Africa, uses the human protein CEACAM6 to gain entry into cells.

Virus Identified in East African Bats

The virus, designated Cardioderma cor coronavirus KY43 (CcCoV-KY43), was originally isolated from heart-nosed bats in Kenya. Researchers did not operate with live virus but instead synthesized the spike protein from genetic sequences obtained from public databases. This approach allowed them to safely assess the virus’s ability to interact with human receptors.

Mechanism of Cellular Entry

Using a recombinant receptor-binding domain (RBD) of the viral spike protein and a human receptor screening platform, scientists found that CcCoV-KY43 binds directly to three members of the carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family: CEACAM3, CEACAM5, and CEACAM6. Further investigation revealed that overexpression of human CEACAM6—a protein abundantly expressed in the respiratory tract—enabled otherwise resistant human cells to support viral entry.

Structural analysis via X-ray crystallography confirmed that the viral RBD binds specifically to the amino-terminal immunoglobulin variable-like (IgV) domain of human CEACAM6. This interaction represents a previously unrecognized pathway for coronavirus entry into human cells.

Broader Implications for Coronavirus Spillover Risk

The study extended beyond CcCoV-KY43 to examine related viruses. Two other coronaviruses isolated from the same bat species in Kenya were also found to use human CEACAM6 as a receptor. In contrast, viruses from horseshoe bats (Rhinolophus spp.) in Russia and China showed more restricted usage of non-human forms of CEACAM6.

These findings suggest that the ability to use CEACAM6 as a receptor may be more widespread among alphacoronaviruses than previously appreciated, particularly those circulating in East African bat populations.

No Current Evidence of Human Infection

Despite the virus’s ability to enter human cells in laboratory settings, there is no indication that it has spilled over into human populations. Immune surveillance using blood serum samples from individuals living near the sampling sites in Kenya’s Taveta region showed no significant antibodies against CcCoV-KY43, suggesting limited or no recent human exposure.

Researchers emphasize that while the virus possesses the molecular machinery to infect human cells, spillover depends on numerous ecological and epidemiological factors, and current evidence does not support ongoing transmission to people.

Significance for Pandemic Preparedness

Identifying novel receptor usage patterns in animal viruses is a critical step in anticipating zoonotic threats. By revealing that alphacoronaviruses can exploit CEACAM6—a protein involved in cancer biology and immune regulation—this study expands the known landscape of coronavirus-host interactions. Such insights improve surveillance strategies and inform risk assessment for future spillover events.

The collaborative effort included researchers from the University of York, the University of Cambridge, The Pirbright Institute, the KEMRI-Wellcome Trust Research Programme, and the National Museums of Kenya, highlighting the importance of global partnerships in emerging infectious disease research.

Key Takeaways

• A bat coronavirus (CcCoV-KY43) from East Africa can bind to the human receptor CEACAM6 to enter cells.
• The interaction occurs via the viral spike protein’s receptor-binding domain attaching to the IgV domain of CEACAM6.
• Two related viruses from the same region also use CEACAM6, suggesting broader potential among African alphacoronaviruses.
• No serological evidence indicates recent human infection in the communities where the virus was sampled.
• Understanding alternative receptor pathways enhances pandemic preparedness by revealing hidden risks in viral reservoirs.