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Lecture 2

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McGill University
Microbiology and Immun (Sci)
MIMM 465
Edith Zorychta

Lecture 2 - 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 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 - 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)  However, women can have herpes INSIDE the vagina (on the cervix) w/o any external lesion = more common for the asymptomatic women to infect men THAN vice versa Baby with herpes neonatorum – disseminated cutaneous infection of herpes - Baby was born through a birth canal with a woman who has the virus - This is rarely seen nowadays Herpetic Whitlow - Herpes on the finger Public toilet could transmit herpes? – A bit of myth - Viruses NEED the warm and intimate contact b/c they are so fragile  Die or dry out when viruses reach to room temperature - EXTREMELY rare to transmit herpes through the public toilet VZV – causes 2 diseases - Varicella (chickenpox)  A primary infection  Always disseminated - Zoster (shingles)  A local recurrence of latent infection (NOT a primary infection) Transmission - Through the vesicle fluid and respiratory secretion - 14-15 days incubation period - Highly contagious w/in households and schools - In absence of vaccination  Primary varicella occurs in 50-80% by age 6  80-95% of adults are seropositive (immune) – they were infected as children  Among seropositive adults – only 80-90% give a history of ever having the varicella b/c severity of varicella is inversely proportional to age - Many cases of varicella re mild or even inapparent - Generally, varicella is MORE severe in adult than children  Sick for about 2 weeks when you have varicella - Primary infection, recovery and seropositivity – primary infection provides absolute immunity to reinfection - All subsequent manifestations in ppl who had a primary infection represent reactivation of latent virus from sensory ganglia Manifestations of varicella (chickenpox) - Fever, chills, myalgias (muscle aches) - Rash may come in success crops of vesicles and usually resolves over 7-14 days - Illness usually relatively mild in young children - Children may have only 3-10 vesicles - Illness is usually more sever in adults – not uncommon for adults to have >1000 vesicles - Progressive varicella  Pneumonia, meningoencephalitis, hepatitis, etc  Rare in healthy ppl but many occur in 10-20% of pregnant women  Varicella immune titer is done to screen women who want to get pregnant – if they aren’t immune then they get vaccinated before they get pregnant - If they are already pregnant, then they should AVOID the cases of varicella - If they contact the varicella WHILE the pregnancy – passive immunity shots given Zoster (shingles) - Zoster is a localized recurrence in a unilateral (one-sided) sensory dermatome - Heralded by 2-3 days of pain prior to onset of visible skin lesions - Major manifestations are pain, itch and visible vesicles - Healing time is variable with a range from 5 days to >30 days - Incidence and severity proportional to age - Recurrence disease that occurs more in older ppl CNS - Anterior and posterior nerve roots in spinal cord that combine to form the combined spinal nerve root  Posterior root is sensory - Neurons that leave the spinal cord and synapse with the peripheral sensory nerve in the spinal ganglion - Spina
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