1- Viral lymphadenitis (HIV-EBV)

Viral lymphadenitis
Dr/ Nahed Fathallah Fahmy

ILOs
 Definition and the aetiology of viral
lymphadenitis
 General features and pathogenesis of the
causative organisms
Definition
 Viral Lymphadenitis means inflammation and enlargement of
lymph nodes duo to viral infection which may be localized or
generalized.
Causative viruses;
 Herpesviruses;
• Epstein barr virus
• Cytomegalovirus
• Human herpes virus 6
 Retroviruses;
• Human immunodeficiency virus
 Rubella virus
 Adenoviruses
Human immunodeficiency virus HIV
Structure;
The virus is spherical composed of cylinderical internal core of
proteins.
Core: The most important core protein is (p24=the capsid). It
appears in the serum early after infection, serological marker for
virus replication. The core contains two identical copies of
positive sense ssRNA genome. Enzymes: reverse transcriptase,
integrase and protease.
Viral envelope composed of lipid bilayer contains precursor

glycoprotein gp160 which is cleaved to form two envelope type
specific glycoproteins gp120, gp41
gp 120 protrude from the surface interact with CD4 molecules on T cells,
monocytes, macrophages, dendritic cells.
gp 41 is a transmembrane protein stem embedded in the envelope.
HIV Replication
- Binding of gp120 to
CD4 protein and coreceptors
on the cell surface.
 Gp41 mediate fusion of
viral envelope with the cell
membrane virus enter cell.
HIV Replication
 After uncoating, RT transcribes the genome RNA into double

stranded DNA (provirus) which intergrates into the host cell DNA
by the action of integrase.
HIV Replication
 Viral mRNA transcribed from

the proviral DNA and
transported to the cytoplasm
where it is translated into large
polyprotein .
 Polyproteins cleaved by
protease enzyme to produce
different viral structure and
enzymes during viral assembly
and budding from the cell.
Transmission
*Blood, semen,vaginal secretions
 Sexual contact
 Exposure to contaminated blood and blood

products
 From infected mother to her baby perinatally
Pathogenesis & immunity
 CD4 molecules are major receptors for
attachment of viral gp120.
 T helper cells. Monocytes, macrophages,
dendritic cells express CD4 surface molecules
and infected by the virus.
 During acute stage , CD8 cytotoxic cells and antibodies
dramatically reduce HIV level , then the virus escapes
from the immune system and establish chronic latent
infection through;
1. Viral mechanisms:
 latent infection of host cells as a provirus,
 rapid genetic mutations,
 trapping of infectious virus in lymphoid tissues act
as a reservoir.
2. Suppression of immune mechanisms:
 Deletion of CD4 T cells , deletion of HIV CTL clones,
 dysfunction of CTL duo to decreased production of IL2, decreased
expression of MHC1 by viral genes,
 interferance with humoral response which is T cell dependant.
Clinical finding
1. Acute stage:
 infectious mononucleosis sydrome like findings occur
2-4 weeks after infection:
 Generalized lymphadenopathy, fever, sore throat, rash
 Resolve spontaneously in 2 weeks, antibodies to HIV
appear 3-4 weeks after infection
 Rapid replication of virus, disseminate to various
organs lymph nodes
 Immune response by CTL, humoral immunity control
infection.
2. Clinical latency (up to 10 years)
Patient is Asymptomatic, low vireamia,
virus produced in large quantities and trapped by Follicular
dendritic cells in lymph nodes.
Syndrome AIDS related complex occur characterized by : fever,
persistant lymphadenopathy, progress to AIDS.
3. Late stage: “AIDS” acquired immunodeficiency syndrome
Decline in number of CD4 cells below 400.
 Opportunitic infections:
Bacteria: Mycobacterium avium complex, Mycobacterium tuberculosis
Fungi; Candida, Cryptococcus neoformans
Viruses; cytomegalovirus
 Cancer: lymphoma, kaposi sarcoma.
 Neurological: Neuropathy., encephalopathy, dementia
Laboratory diagnosis
 Decreased CD4 count
 Inverted CD4/CD8 ratio.
 Detection HIV antibodies “p24, gp41, gp120” (6-12 weeks):
 ELISA.
 Positive test confirmed by western blot.
 Detection of viral nucleic acid by quantitative PCR,

 monitor the effectivness of antiviral drugs.
 Detection of viral antigens p24 by ELISA:
 Only marker in window phase early in infection when
antibodies are not detected.
 P24 become undetectable after antibodies appear.
 P24 reappear late indicating poor prognosis.
 Virus isolation.
Epstein barr virus
Properties;
*viral Antigens;
- Viral capsid antigen (VCA)
- Early antigen (EA)
- Nuclear antigen (EBNA)
- Viral membrane antigen (MA)
• It infect B cells and remain latent
• Viral DNA integrates into the cell genome
• EBV transform B cells in vitro, they become
immortal, proliferate indefinitely
 Pathogenesis;
• EBV transmitted by saliva
• Infection starts in the oropharynx then spread to blood ,
virus infect B lymphocytes
 Clinical finding;
• In children; primary infection asymptomatic.
• In adolescents; manifest with infectious mononucleosis:
• Polyclonal activation of of B cells which secrete autoimmune
heterophil antibodies.
• Disease characterized by fever, sore throat, lymphadenopathy,
rash
Tumors;
• Burkitts lymphoma
• Nasopharyngeal carcinoma.
Oral hairy leukoplakia in AIDS patients
Diagnosis
 Blood picture;
• Increase leukocytic count
• Absolute lymphocytosis
• Atypical lymphocytes (cytotoxic T lymphocytes react
against infected B cells which change in morphology)
 Detection of nucleic acid of EBV in saliva, throat washing by
PCR.
 Detection of antibodies to EBV by ELISA (IgM to VCA
indicates recent infection)
 Mono spot test to detect heterophil antibodies that agglutinate
sheep RBCs
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Viral lymphadenitis

Dr/ Nahed Fathallah Fahmy

• Human herpes virus 6

Viral envelope composed of lipid bilayer contains precursor

 After uncoating, RT transcribes the genome RNA into double

 Viral mRNA transcribed from

 Exposure to contaminated blood and blood

 Positive test confirmed by western blot.

 Detection of viral nucleic acid by quantitative PCR,

 P24 reappear late indicating poor prognosis.

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