Viral protein protects EBV-infected B cells

An EBV-infected cell (green)

expresses the ligand (red)

that activates NKG2D, while

uninfected cells (blue) do not

Benjamin Chaigne-Delalande

A study published in PLOS Pathogens sheds new light on why the immune system cannot eliminate Epstein-Barr virus (EBV) or the risk of cancer associated with the virus.

Researchers investigated the immune system’s response against EBV, focusing on the role of LMP2A.

This viral protein is present in latently infected B cells and in many EBV-associated cancers, which have somehow escaped detection and elimination by the immune system.

Andreas Moosmann, PhD, of the Helmholtz-Zentrum in Munich, Germany, and his colleagues studied an engineered EBV virus that cannot make LMP2A and compared this mutant virus with the normal one.

The researchers infected human B cells with normal and LMP2A-deficient EBV. Because EBV transforms these cells, the team was able to examine lymphoblastic cell lines that contained either virus.

They found that LMP2A counteracts the recognition of EBV-infected B cells by EBV-specific, CD8⁺ killer T cells. In contrast, EBV-transformed cells without LMP2A are more efficiently identified, and the T cells’ ability to recognize and kill the EBV-infected B cells is enhanced.

The researchers examined the mechanism underlying the LMP2A-mediated evasion and found several ways in which it interferes with the recognition of EBV-infected cells.

First, LMP2A reduced the levels of several EBV proteins whose fragments are recognized by CD8⁺ T cells on the surface of the cell targeted for killing.

Second, LMP2A disturbs the expression of cellular molecules on infected B cells that interact with NKG2D, a host molecule on the surface of CD8⁺ T cells that aids their activation, thereby weakening the immune response against EBV-infected cells.

The researchers said these results suggest a functional immunomodulatory effect for the EBV protein LMP2A and show that LMP2A mediates the partial escape of infected B cells from recognition by CD8⁺ T cells.

The team also said similar immune evasion mechanisms may operate in different types of LMP2A-expressing cancers caused by EBV.

An EBV-infected cell (green)

expresses the ligand (red)

that activates NKG2D, while

uninfected cells (blue) do not

Benjamin Chaigne-Delalande

A study published in PLOS Pathogens sheds new light on why the immune system cannot eliminate Epstein-Barr virus (EBV) or the risk of cancer associated with the virus.

Researchers investigated the immune system’s response against EBV, focusing on the role of LMP2A.

This viral protein is present in latently infected B cells and in many EBV-associated cancers, which have somehow escaped detection and elimination by the immune system.

Andreas Moosmann, PhD, of the Helmholtz-Zentrum in Munich, Germany, and his colleagues studied an engineered EBV virus that cannot make LMP2A and compared this mutant virus with the normal one.

The researchers infected human B cells with normal and LMP2A-deficient EBV. Because EBV transforms these cells, the team was able to examine lymphoblastic cell lines that contained either virus.

They found that LMP2A counteracts the recognition of EBV-infected B cells by EBV-specific, CD8⁺ killer T cells. In contrast, EBV-transformed cells without LMP2A are more efficiently identified, and the T cells’ ability to recognize and kill the EBV-infected B cells is enhanced.

The researchers examined the mechanism underlying the LMP2A-mediated evasion and found several ways in which it interferes with the recognition of EBV-infected cells.

First, LMP2A reduced the levels of several EBV proteins whose fragments are recognized by CD8⁺ T cells on the surface of the cell targeted for killing.

Second, LMP2A disturbs the expression of cellular molecules on infected B cells that interact with NKG2D, a host molecule on the surface of CD8⁺ T cells that aids their activation, thereby weakening the immune response against EBV-infected cells.

The researchers said these results suggest a functional immunomodulatory effect for the EBV protein LMP2A and show that LMP2A mediates the partial escape of infected B cells from recognition by CD8⁺ T cells.

The team also said similar immune evasion mechanisms may operate in different types of LMP2A-expressing cancers caused by EBV.

An EBV-infected cell (green)

expresses the ligand (red)

that activates NKG2D, while

uninfected cells (blue) do not

Benjamin Chaigne-Delalande

A study published in PLOS Pathogens sheds new light on why the immune system cannot eliminate Epstein-Barr virus (EBV) or the risk of cancer associated with the virus.

Researchers investigated the immune system’s response against EBV, focusing on the role of LMP2A.

This viral protein is present in latently infected B cells and in many EBV-associated cancers, which have somehow escaped detection and elimination by the immune system.

Andreas Moosmann, PhD, of the Helmholtz-Zentrum in Munich, Germany, and his colleagues studied an engineered EBV virus that cannot make LMP2A and compared this mutant virus with the normal one.

The researchers infected human B cells with normal and LMP2A-deficient EBV. Because EBV transforms these cells, the team was able to examine lymphoblastic cell lines that contained either virus.

They found that LMP2A counteracts the recognition of EBV-infected B cells by EBV-specific, CD8⁺ killer T cells. In contrast, EBV-transformed cells without LMP2A are more efficiently identified, and the T cells’ ability to recognize and kill the EBV-infected B cells is enhanced.

The researchers examined the mechanism underlying the LMP2A-mediated evasion and found several ways in which it interferes with the recognition of EBV-infected cells.

First, LMP2A reduced the levels of several EBV proteins whose fragments are recognized by CD8⁺ T cells on the surface of the cell targeted for killing.

Second, LMP2A disturbs the expression of cellular molecules on infected B cells that interact with NKG2D, a host molecule on the surface of CD8⁺ T cells that aids their activation, thereby weakening the immune response against EBV-infected cells.

The researchers said these results suggest a functional immunomodulatory effect for the EBV protein LMP2A and show that LMP2A mediates the partial escape of infected B cells from recognition by CD8⁺ T cells.

The team also said similar immune evasion mechanisms may operate in different types of LMP2A-expressing cancers caused by EBV.