Herpes simplex virus

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Herpes simplex virus

Unit 7 Nervous

Unit 7 Nervous

Headaches: Clinical
Headaches: Pathology review
Migraine medications
Migraine
Central nervous system histology
Peripheral nervous system histology
Development of the nervous system
Ascending and descending spinal tracts
Brown-Sequard Syndrome
Syringomyelia
Anatomy of the trigeminal nerve (CN V)
Anatomy of the basal ganglia
Anatomy of the white matter tracts
Anatomy clinical correlates: Vertebral canal
Anatomy of the cerebral cortex
Anatomy of the cerebellum
Basal ganglia: Direct and indirect pathway of movement
Cerebrospinal fluid
Blood brain barrier
Dandy-Walker malformation
Intracerebral hemorrhage
Subdural hematoma
Epidural hematoma
Subarachnoid hemorrhage
Shaken baby syndrome
Normal pressure hydrocephalus
Huntington disease
Movement disorders: Pathology review
Anti-parkinson medications
Parkinson disease
Cluster headache
Tension headache
Chiari malformation
Spina bifida
Cerebral circulation
Cerebellum
Glaucoma
Eye conditions: Refractive errors, lens disorders and glaucoma: Pathology review
Anatomy and physiology of the eye
Anatomy of the eye
Anatomy of the oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
Eye and ear histology
Anatomy and physiology of the ear
Auditory transduction and pathways
Vestibular transduction
Vertigo: Pathology review
Dizziness and vertigo: Clinical
Otitis media
Pediatric ear, nose, and throat conditions: Clinical
Optic pathways and visual fields
Photoreception
Eye conditions: Retinal disorders: Pathology review
Eye conditions: Inflammation, infections and trauma: Pathology review
Taste and the tongue
Olfactory transduction and pathways
Anatomy of the tongue
Meningitis
Meningitis, encephalitis and brain abscesses: Clinical
Neisseria meningitidis
Mumps virus
Herpes simplex virus
Poliovirus
West Nile virus
West Nile Virus Infection
Trypanosoma cruzi (Chagas disease)
Seizures and epilepsy
Early infantile epileptic encephalopathy (NORD)
Febrile seizure
Seizures: Clinical
Seizures: Pathology review
Nonbenzodiazepine anticonvulsants
Anticonvulsants and anxiolytics: Benzodiazepines
Anticonvulsants and anxiolytics: Barbiturates
Cranial nerves
Cranial nerves rap
Introduction to the cranial nerves
Cranial nerve pathways
Brain tumors: Clinical
Pediatric brain tumors: Pathology review
Adult brain tumors: Pathology review
Knowledge Shot: Glioblastoma
Adult brain tumors
Tuberous sclerosis
von Hippel-Lindau disease
Neurofibromatosis
Anatomy of the limbic system
Schizophrenia
Schizophrenia spectrum disorders: Clinical
Schizophrenia spectrum disorders: Pathology review
Anatomy of the vertebral canal
Anatomy clinical correlates: Spinal cord pathways
Anatomy of the olfactory (CN I) and optic (CN II) nerves
Anatomy of the facial nerve (CN VII)
Anatomy of the glossopharyngeal nerve (CN IX)
Anatomy of the spinal accessory (CN XI) and hypoglossal (CN XII) nerves
Anatomy of the vagus nerve (CN X)
Ischemic stroke
Restless legs syndrome
Acoustic neuroma (schwannoma)
Pediatric brain tumors
Pituitary adenoma
Cauda equina syndrome
Neonatal meningitis
Encephalitis
Bell palsy
Cerebral vascular disease: Pathology review
Spinal cord disorders: Pathology review
Dementia: Pathology review
Anatomy of the inner ear
Emotion
Stroke: Clinical
Broca aphasia
Wernicke aphasia
Delirium
Dementia and delirium: Clinical
Medications for neurodegenerative diseases
General anesthetics
Sleep
Dementia with Lewy bodies
Tricyclic antidepressants
Alzheimer disease
Frontotemporal dementia

Transcript

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Most of the time, when herpes simplex virus or HSV infects a person, there are no symptoms.

In fact, it also usually moves from one person to another in the absence of symptoms, so it can therefore it can move through a population silently.

Once in a while, though, it can cause symptoms, and typically those are in the form of skin and mucous membrane lesions which can be divided into infections “above the waist”—mostly involving the mouth and tongue, and those “below the waist”—involving the genitals.

There are two types of herpes simplex viruses—HSV1 and HSV2—both of which are part of a larger family of enveloped double-stranded DNA viruses: the herpesviridae family.

Generally speaking, HSV1 tends to cause infections above the waist and HSV2 tends to cause infections below the waist, but there’s a lot of crossover because both viruses can cause both types of infections.

Although herpes is most contagious when there are virus-filled lesions present, it can also spread by asymptomatic shedding which means that herpes viruses can be in saliva or genital secretions even when there are no signs of a cold sore or genital lesion.

Typically, when herpes virus lands on a new host, in other words a person that’s never had herpes before, it dives into small cracks in the skin or mucosa and binds to epithelial cell receptors, which triggers those cells to internalize the virus.

Once inside, the virus starts up the lytic cycle, which is where its DNA gets transcribed and translated by cellular enzymes which help to form viral proteins which are packaged into new herpes viruses which can leave to go off and infect neighbouring epithelial cells.

HSV1 and HSV2 also infect nearby sensory neurons, and travel up their axon to the neuron’s cell body to start up the latent cycle.

The sensory neurons of the face have their cell bodies in the trigeminal nuclei and those around the genitalia are located in the sacral nuclei.

So that’s ultimately where the herpes virus settles in—for life!

You see, the sensory neurons aren’t destroyed, instead, they become a permanent home for the herpes virus, and from time to time, the herpes virus makes a few viral copies of itself and sends those virus particles back down the axon so they can get released and infect epithelial cells.

Since the trigeminal and sacral nuclei serve just one side of the face or body, herpes vesicles and ulcers develop on the ipsilateral or same side as the affected nuclei.

This can happen over and over again throughout a person’s lifetime, with classic triggers being things like stress, skin damage, and viral illnesses.

Recurrent episodes are usually less severe than the primary infection, and sometimes there are no symptoms at all.

When there are symptoms, there might be a characteristic tingling or burning sensation, called a prodrome, one or two days before the blisters appear.

In oral and genital herpes, the primary infection is most often asymptomatic.

Having said that, in oral herpes when it does cause symptoms it usually affects children and it causes lesions on the palate, gums, tongue, lip, and facial area, as well as a fever and enlarged lymph nodes.

The lesions themselves are typically clusters of small, painful, fluid-filled blisters, that ooze and ulcerate, and then eventually heal after a few weeks.

In older children and adults, a common symptom is pharyngitis.

Most of the time, like primary infection, reactivation doesn’t cause any symptoms, but when it does, the most common pattern is having a handful of blisters at the vermillion border—the border of the lip—on one side of the face.

These blisters are typically smaller and heal over a week.

With genital herpes, primary infection can cause symptoms like ulcers and pustules which form on the labia majora, labia minora, mons pubis, vaginal mucosa, and cervix in women and on the shaft of the penis in men.