BIOL 374: Molecular Biology Lab
Lab 10: The impact of primary EBV infection on primary B cellular transcriptomes
BIOL 374 Molecular Bio Lab 10: EBV primary infection & the host transcriptome page 1 Dr. Vanderlaan | Dr. Gacura
BACKGROUND:
Viral encephalitis
Viral encephalitis is an inflammation of the brain caused by viral infection, leading to swelling, neuronal damage, and
potentially life-threatening complications (1). In neonates, it is particularly dangerous because their immune systems are
immature, making them less able to control viral spread (1). Additionally, their blood-brain barrier is more permeable,
allowing viruses easier access to the central nervous system, which can result in seizures, developmental delays, or death
if not promptly treated. In pediatric cases, infectious viral agents are recognized contributors not only to viral encephalitis
but also to a range of clinical symptoms that can mimic signs of child neglect, such as failure-to-thrive (FTT), involuntary
convulsions, and seizures (1). These viruses include several herpesviruses, notably herpes simplex virus-1 (HSV-1) and HSV-
2, varicella-zoster virus (VZV or chickenpox), human herpesvirus 4 (HHV-4 or Epstein-Barr virus or EBV), human
herpesvirus 5 (HHV-5 or cytomegalovirus or CMV), and human herpesvirus 6 (HHV-6 or roseolovirus) (1).
Human oncoviruses
Human oncoviruses are viruses known to contribute to the development of cancer through chronic infection, immune
evasion, and disruption of normal cellular control mechanisms (Figure 10-1) (2,3). For instance, Epstein-Barr virus (EBV)
is a herpesvirus linked to several lymphomas, including Burkitt lymphoma and Hodgkin lymphoma, as well as
nasopharyngeal carcinoma (4–11). Hepatitis B virus (HBV) and Hepatitis C virus (HCV) both cause chronic liver infections
that can progress to cirrhosis and hepatocellular carcinoma (2,3). Human herpesvirus 8 (HHV-8) is associated with Kaposi’s
sarcoma, particularly in immunocompromised individuals (2,3). Human papillomavirus (HPV), especially high-risk types
like HPV-16 and HPV-18, is a major cause of cervical, anal, and oropharyngeal cancers through the action of viral oncogenes
that inactivate tumor suppressor proteins (2,3). Human T-lymphotropic virus type 1 (HTLV-1) causes adult T-cell
leukemia/lymphoma by integrating into host DNA and promoting uncontrolled T-cell proliferation (2,3). Lastly, Merkel cell
polyomavirus (MCPyV) has been implicated in the development of Merkel cell carcinoma, a rare but aggressive skin cancer,
particularly in the elderly and immunosuppressed (2,3). Oncoviruses leverage multi-hit models of oncogenic
transformation in target cells (Figure 10-2) (2,3,12).
Figure 10-1. The human oncovirus landscape.
