Epstein-Barr virus infection at mucosal surfaces: detection of genomic variants with altered pathogenic potential

Sixbey, John W.; Shirley, Pam

doi:10.1007/bf00201467

Cited by 4 publications

(1 citation statement)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[17][18][19][20] EBV enters via the oropharynx, where the lytic phase with viral replication occurs in the epithelial cells. 21 However, some studies suggest that B cells of the oropharynx might be the primary infected cells. 22 …”

Section: Cellular Infectionmentioning

confidence: 99%

Epstein–Barr Virus in Cutaneous Pathology

Fernández-Flores

2013

The American Journal of Dermatopathology

View full text Add to dashboard Cite

Epstein-Barr virus (EBV) is a ubiquitous double-stranded DNA gamma herpes virus and it is present in 95% of adults. EBV infection is seen in many oncological conditions, although there is controversy regarding whether EBV is causative, a cofactor, or just a coincidental infection. Some of these conditions involve the skin as the main or as a secondary organ. In this report, we review several tumoral and nontumoral cutaneous conditions, which are related to EBV infection, and describe the epidemiology of infection and the life cycle of the virus.

show abstract

Section: Cellular Infectionmentioning

confidence: 99%

Epstein–Barr Virus in Cutaneous Pathology

Fernández-Flores

2013

The American Journal of Dermatopathology

View full text Add to dashboard Cite

show abstract

Epstein–Barr virus: Dermatologic associations and implications

Hall,

Eminger,

Hesterman

et al. 2015

Journal of the American Academy of Dermatology

View full text Add to dashboard Cite

Epstein-Barr Virus BALF1 Is a BCL-2-Like Antagonist of the Herpesvirus Antiapoptotic BCL-2 Proteins

Bellows¹,

Howell

Pearson

et al. 2002

J Virol

View full text Add to dashboard Cite

Cellular BCL-2 family proteins can inhibit or induce programmed cell death in part by counteracting the activity of other BCL-2 family members. All sequenced gammaherpesviruses encode a BCL-2 homologue that potently inhibits apoptosis and apparently escapes some of the regulatory mechanisms that govern the functions of their cellular counterparts. Examples of these protective proteins include BHRF1 of Epstein-Barr virus (EBV) and KSBcl-2 of Kaposi's sarcoma-associated herpesvirus, also known as human herpesvirus 8. The gamma-1 subgroup of these viruses, such as EBV, encodes a second BCL-2 homologue. We have now found that this second BCL-2 homologue encoded by EBV, BALF1, inhibits the antiapoptotic activity of EBV BHRF1 and of KSBcl-2 in several transfected cell lines. However, BALF1 failed to inhibit the cellular BCL-2 family member, BCL-x L . Thus, BALF1 acts as a negative regulator of the survival function of BHRF1, similar to the counterbalance observed between cellular BCL-2 family members. Unlike the cellular BCL-2 family antagonists, BALF1 lacked proapoptotic activity and could not be converted into a proapoptotic factor in a manner similar to cellular BCL-2 proteins by caspase cleavage or truncation of the N terminus. Coimmunoprecipitation experiments and immunofluorescence assays suggest that a minimal amount, if any, of the BHRF1 and BALF1 proteins colocalizes inside cells, suggesting that mechanisms other than direct interaction explain the suppressive function of BALF1.

show abstract

Epstein-Barr virus infection at mucosal surfaces: detection of genomic variants with altered pathogenic potential

Cited by 4 publications

References 69 publications

Epstein–Barr Virus in Cutaneous Pathology

Epstein–Barr Virus in Cutaneous Pathology

Epstein–Barr virus: Dermatologic associations and implications

Epstein-Barr Virus BALF1 Is a BCL-2-Like Antagonist of the Herpesvirus Antiapoptotic BCL-2 Proteins

Contact Info

Product

Resources

About