MIMM 465 Lecture Notes - Lecture 2: Sensory Nerve, Trigeminal Nerve, Guanosine

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Published on 16 Apr 2013
School
McGill University
Department
Microbiology and Immun (Sci)
Course
MIMM 465
Lecture 2
<Herpes Viruses : Replication, Expression, Latency & Clinical Aspects> - Dr. Briedis
Graph of publications per year of all Herpes and Herpes Simplex viruses
- Fewer than 30 publications per year in the 60s and 1000 publications per year in 1975
- Came down again after 1975
- Laboratory science tend to follow fashion b/c of the funding fashion
- In the 60s and 70s, there was a SEXUAL revolution!
As a result, sexually transmitted disease called Herpes Simplex Genitalis was developed
HSV rocketed high, which infects the person for LIFE It was almost conceived as modern day HIV
As a result, ppl started to do research on HSV
Thought of the 60s, was that HSV causes the carcinoma on the cervix however, was simply a correlation of
sexual promiscuity, not a causal relationship
- In 1981, HIV/AIDS broke out and completely took over the funding/research
HSV research plummeted from then
Herpes viruses Structure
- All herpes viruses have identical morphology
- Plasma membrane envelope with glycoproteins in it
Envelope membrane derived from nuclear membrane by
budding
- Internal icosahedral nuclear capsid, containing DNA, with
surrounding tegument proteins and capsid proteins
Icosahedral symmetry of virus capsid
- Large double stranded circular DNA genome w/in the virus
- dsDNA genome 125,000-229,000bp
- 162 capsomeres
Electron micrograph of the Herpes virus
- All human herpes virus look identical under electron microscopy
HSV protein expression:
- Genetically complicated virus
- >100 transcripts with >70 ORFs
All human herpes viruses have identical morphology
- All are ubiquitous, infecting a majority of all humans
Most of the ppl are latently infected with at least 4~6 different human herpes viruses
- All remain latent lifelong and may periodically reactivate with active viral replication
Human herpes viruses 2 classifications
- They were named in a different fashion before..subsequently, there was an agreement in order to RENAME them..
New classification as Human Herpes Virus (HHV)
- HSV type I (HSV1 or HHV1)
- HSV type II (HSV2 or HHV2)
- Varicella-zoster virus (VZV or HHV3)
- Epstein-Barr virus (EBV or HHV4)
- Cytomegalovirus (CMV or HHV5)
- Human herpes virus 6 (HHV6)
- Human herpes virus 6 (HHV7)
- Kaposi sarcoma-associated virus (KSHV or HHV8)
Associated with malignancy with HIV patients
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All of the herpes viruses have tendency to infect tissues and have the specific tropisms
- Particular site of latency and disease for each of the virus
Herpes Virus Type
Tissue Tropism
Site of Latency
Comment
HSV1 & HSV2
Skin, nerves
Sensory neural ganglia
Predominantly labial and genital disease
VZV/HHV3
Skin, nerves
Sensory neural ganglia
Chickenpox (Varicella)
Shingles (Zoster)
EBV/HHV4
B lymphocytes
Lymphoid tissues
Infectious mononucleosis
CMV/HHV5
Multiple tissues
Multiple tissues
Multiple syndromes: perinatal infections &
severe and recurrent disease in compromised
hosts
HHV6
T lymphocytes
Lymphoid
Exanthem subitum (Roseola)
HHV7
T lymphocytes
Lymphoid
Exanthem subitum (Roseola), acute febrile
respiratory disease, drug-induced
hypersensitivity, encephalopathy, hepatitis,
hemiconvulsion-hemiplegia-epilepsy,
reactivation of HHV-4, leading to
mononucleosis-like illness
KSHV/HHV8
Skin, B lymphocytes
Lymphoid
Associated with Kaposi sarcoma, HIV-related
B cell lymphomas, and proliferative skin
disorders in immunocompromised hosts
- CMV is amphitropic, meaning it can infect multiple tissues and stay latent in multiple tissues result of multiple
syndromes (infection in new born and immunocompromised patients)
- HHV6 and HHV7 are similar
Roseola benign rash infection in newborn infants
- It appear to be virus infection but children would get it even if they don’t have a contact with other children
- It was an infectious disease, but was passed from MOTHER to children by the mother’s kisses (saliva)
HHV6/HHV7 PCR of ppl’s blood – 15% of normal population would be positive for circulating HHV6/HHV7
DNA b/c people who are latently infected with the virus have periodic reactivation of the virus
- Small amt of recirculating activated viruses in the bloodstream
- Poor relation of herpes infection with the hepatitis infection
- KSHV or HHV8 many diseases seen uniquely in immunocompromised patients
HSV-1 and HSV-2
- Both have serologically/antigenically distinct membrane
glycoproteins
- Similar manifestations when infecting identical sites
- Different but converging epidemiological patterns
- Labial infection (nongenital) commonly known as
‘mouth/kissing’ infection
Due to the sexual revolution, ppl started to put their
lips on other ppl’s genitals and this resulted in easier
transmission of labial infection of HSV1
- Once you have the lip infection, ppl scratch their mouth and
scratch their eyes ocular keratitis
Similar situation for the hand infection
- Two infections in adults’ CNS – encephalitis and meningitis
Follow different epidemiology b/w HSV1 and HSV2
- Looks like encephalitis is associated with labial/mouth infection (cold sore), while meningitis is associated
with the genital infection
Encephalitis infection of the substance of the brain
Meningitis infection of the membrane surrounding the brain
- These viruses are latent in sensory neural ganglia
When you have mouth/lips infection virus travels up to sensory trigeminal nerve to the trigeminal ganglia
(near the ear) stays latent in that ganglia
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- In this situation (trigeminal ganglia), virus stays close to the brain and retrogrades back along the cranial
nerve and infects the brain substance
When you have urogenital infection virus travels along the sensory nerves through our spinal sensory sacral
ganglia and stays latent there
- Virus only spread hematogenously in the sacral ganglia of the butt, along the bloodstream of the CNS = virus
tend to lodge in the meningeal membrane
- Women with active genital lesions pass the HSV2 to their babies
Manifestation of HSV infection (i.e. Herpes labialis & Herpes genitalis)
- HSV1/HSV2 infection 30~100% of population by age 5
30~50% of middle class children raised at home
80~100% of poorer populations raised at the communal daycare settings
- Children transmit the virus by bodily secretion (saliva)
- Primary infection in children is often asymptomatic but may present as severe gingivostomatitis (gums and the
membrane in the mouth infection)
- Paradoxically
Primary infection is most often asymptomatic BUT when symptomatic, it is usually severe
- Incubation period 2-12 days (relatively short)
- Eye, hand or other skin sites may be infected de novo (primarily) or by autoinoculation mouth and genital are most
common
- In patients w/o immune compromise
Usually no serious sequelae
Treatment is optional
Recurrent infections:
- Occurs in same site as primary infection
Occurs b/c the virus is latent in the trigeminal/sacral nerve ganglia and retrogrades back down the nerve fibers
to the same area of the skin that was close to the place of primary infection
- Latency occurs in sensory ganglia
- Reactivation often attributed to inciting causes
Concurrent infection, fever (blisters)
Stress, Menses, exposure to UV light, etc
- Small quantities of virus may periodically be shed asymptomatically w/o having active lesions
Young boy with primary labial infection
- Can spread certain amount from the lips
Boy with acute lymphocytic leukemia who developed primary severe gingivostomatitis
- Also can spread certain amount
It starts as fluid-filled vesicle blisters
- It breaks open and crusts over painful & sore heals up in a few days
- Recurrence could happen
Psoriasis rash blisters ALL OVER THE BODY
- Herpes can be developed from the recurrence of the primary ocular herpes
- Small amts of virus was shed from the recurrence virus spread to every parts of the body lead to the
dissemination of the herpes
Blisters on genital herpes
- Almost the same blisters of the labial infection
- Flat ulcers could occur
- Edema could occur in the SEVERE case of herpes large inflammation
- Blisters can be developed on the cervix highly infectious with unprotected sex
- Generally when a man has the herpes, 99% of the time he knows about it (due to pain and visible blisters)
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Document Summary

- dr. briedis. Graph of publications per year of all herpes and herpes simplex viruses. Fewer than 30 publications per year in the 60s and 1000 publications per year in 1975. Laboratory science tend to follow fashion b/c of the funding fashion. In the 60s and 70s, there was a sexual revolution! As a result, sexually transmitted disease called herpes simplex genitalis was developed. Hsv rocketed high, which infects the person for life it was almost conceived as modern day hiv. As a result, ppl started to do research on hsv. Thought of the 60s, was that hsv causes the carcinoma on the cervix however, was simply a correlation of sexual promiscuity, not a causal relationship. In 1981, hiv/aids broke out and completely took over the funding/research. Plasma membrane envelope with glycoproteins in it. Envelope membrane derived from nuclear membrane by budding.

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