GROUP B PRESENTATION

Main presenters
1. Isaac Kiprop SB11/JR/MN/15766/2022
2. Weldon sang SB11/JR/MN/14117/2022
3. Vincent Mayoyo SB11/JR/MN/14164/2022
4.Joseph Odhiambo SB11/JR/MN/14147/2022
5. Ryan Korir SB11/JP/MN/16711/2022
6. Justin Mutua SB11/JR/MN/14094/2022
HERPES
VIRUS
 INTRODUCTION

What is herpes simplex?

 The herpes simplex virus, also known as HSV, is a viral infection that causes genital and 
oral herpes.
 Many people live with asymptomatic HSV, which means they have the virus without ever having
an outbreak or active episode of herpes.
 Others might experience occasional episodes of small, fluid-filled blisters or sores. These blisters
most commonly appear on the genitals or mouth and lips, but they can also show up on 
hands or fingers and other parts of your body.
 HSV can be sexually transmitted, but the virus can also be transmitted in other ways. There’s a lot
of stigma around herpes, but the virus is actually very common — and nothing to be ashamed of.
According to estimates from the World Health OrganizationTrusted Source:
•about 67 percent of the world’s population under age 50 had oral or genital HSV-1 in 2016
•about 13 percent of people between the ages of 15 and 49 had HSV-2 in 2016
Other research notes that over 90 percent of adults have HSV-1 antibodies by the time they reach their 50s.
Experts have yet to find a cure for herpes, but antivirals and home remedies can help ease the severity of
symptoms. Antiviral medication may also lead to fewer herpes episodes.
Read on to learn more about the difference between HSV-1 and HSV-2, plus get the details on key signs,
diagnosis, and treatment.
DIFFERENCES BETWEEN HERPS-1 AND HERPS-2
There are two main types of the herpes simplex virus: HSV-1 and HSV-2.
HSV-1. This type primarily causes oral herpes, characterized by cold sores or fever blisters that
appear around your mouth or on your face.
HSV-2. This primarily causes genital herpes, which involves sores that appear on or around your
genitals, anus, buttocks, and inner thighs. Sores can also develop inside the vagina.
It’s important to understand that, while HSV-1 is usually associated with cold sores and HSV-2 is
usually associated with genital herpes, both types of the virus can be transmitted through oral or
genital contact.

In short, both HSV-1 and HSV-2 can cause oral and genital herpes episodes.
Many people living with genital herpes actually have HSV-1, since the virus can easily be
transmitted through oral-to-genital contact.
HSV-2 less commonly Trusted Source causes oral episodes, or cold sores, but it’s still possible.
CAUSES OF HERPES VIRUS

 HSV is a contagious virus that can be transmitted through direct contact with sores.
 That said, since the virus also “sheds” on a small percentage of days, it’s possible to
transmit or contract HSV even when symptoms aren’t present. In fact, many people
contract HSV from people who don’t know they have the virus.
 GENERAL BIOLOGIC PROPERTIES
 The human herpesviruses share four significant biologic properties;
1) All of the herpesviruses code for unique enzymes involved in the
biosynthesis of viral nucleic acids. These enzymes are structurally diverse
and parenthetically provide unique sites for inhibition by antiviral agents.
2) The synthesis and assembly of viral DNA is initiated in the nucleus.
Assembly of the capsid is also initiated in the nucleus.
3) Release of progeny virus from the infected cell is accompanied by cell death.
4) All herpesviruses establish latent infection within tissues that are
characteristic for each virus, reflecting the unique tissue trophism of each
member of this family.
STRUCTURE OF HERPES VIRUS
Herpesviruses have a unique four-layered structure:
A core containing the large.
 Double-stranded DNA genome enclosed by an icosapentahedral
capsid which is composed of capsomers.
 The capsid is surrounded by an amorphous protein coat called
the tegument.
 It is encased in a glycoprotein-bearing lipid bilayer envelope.
Herpes virus is in family Herpesviridae based on its structure. These viruses
contain double-stranded DNA which is located at the central core.
Herpesvirus DNA varies in molecular weight from approximately 80 to 150
million, or 120 to 250 kilobase pairs, depending on the virus.
This DNA core is surrounded by a capsid which consists of 162 capsomers,
arranged in icosapentahedral symmetry. The capsid is approximately 100 to 110
nanometers in diameter.
Tightly adherent to the capsid is the tegument, which appears to consist of
amorphous material.
Loosely surrounding the capsid and tegument is a lipid bilayer envelope derived
from host cell membranes.
The envelope consists of polyamines, lipids, and glycoproteins. These
glycoproteins confer distinctive properties to each virus and provide unique
antigens to which the host is capable of responding.
A fascinating feature of herpesvirus DNA is its genomic sequence arrangement.
HERPES VIRUS GENOMES
Herpesviruses can be divided into six groups arbitrarily classified A to F.
 For those herpesviruses which infect humans (group C, group D, and group E)
unique structures are demonstrable.
In the group C genomes, as exemplified by Epstein-Barr virus and the newly
identified Kaposi's sarcoma herpesvirus, the number of terminal reiterations
divides the genome into several well-delineated domains.
The group D genomes, such as varicella-zoster virus, have sequences from one
terminus repeated in an inverted orientation internally. Thus, the DNA extracted
from these virions consist of two equal molar populations.
For group E viral genomes, such as herpes simplex virus and cytomegalovirus,
the genomes are divided into internal unique sequences whereby both termini
are repeated in an inverted orientation. Thus, the genomes can form four
equimolar populations which differ in relative orientation of the two unique
segments.
STRUCTURE OF HERPES VIRUS
 HSV-1
 You can transmit or contract HSV-1, or oral herpes, through direct contact with a herpes sore, saliva, or other bodily
secretions during an episode. If you’re shedding the virus, someone can contract it through direct contact with the site of
the infection.
 Examples of direct contact include:
• kissing
• oral sex
• other skin-to-skin contact
 In other words, if you touch a partner’s cold sore and then touch your own face or genitals shortly afterward, you could
contract the virus. Many children contract the virus after being kissed or touched on the face by an adult with a cold sore.
 The virus can, in theory, be transmitted through shared lip balm, razors, or drinkware and eating utensils, but this is 
pretty rare — older estimates suggest the virus can only live outside your body for a few hours to a few daysTrusted
Source.
 To put it another way, if someone with a cold sore drank from a glass and immediately handed it to you, and you then put
your mouth to the same place on the glass, you could potentially contract herpes. But the chances of that happening are
fairly low.
 Most of the time, the virus is transmitted through contact with sores or the site of the infection during viral shedding.
 HSV-2
 As with HSV-1, you can transmit or contract HSV-2, or genital herpes, through direct contact with a
herpes sore, saliva, or other bodily secretions during an episode. HSV-2 can also be transmitted during
viral shedding.
 Direct contact might include:
a) kissing
b) oral sex
c) Sharing sex toys during a sexual encounter
d) penetrative sex
e) other skin-to-skin contact at the infection site
 Remember: Though many people think of HSV-1 as oral herpes and HSV-2 as genital herpes, both types
of the virus can cause oral or genital episodes.
 RISK FACTORS
Who is at risk for developing herpes simplex infections?
 Anyone can contract HSV, regardless of age. If you’re exposed to HSV, you’re likely to contract the virus.
 Remember, HSV is very common. But because it’s often asymptomatic, plenty of people living with the virus never
have an episode or realize they’ve contracted HSV.
 You may have a higher chance of contracting the virus if you:
 have a sexual partner who lives with HSV
 were assigned female at birth (AFAB). EvidenceTrusted Source suggests more AFAB folks than people
assigned male at birth develop HSV, but this could also mean AFAB folks are more likely to experience
symptoms.
 are immunocompromised
 Some older research suggests HSV-1 antibodies may offer AFAB folks some protection against contracting HSV-2.
Still, many people living with one type of the virus do contract the other typeTrusted Source later on. You won’t
contract the same type of the virus again, though, since it remains dormant in your body once you acquire it.
 You may have a slightly higher chance of contracting genital HSV if you have sex without using condoms or other
barrier methods. Keep in mind, though, that condoms and other barrier methods won’t always cover the infection
site, since sores can appear on the buttocks or inner thighs.
 SYMPTOMS OF HERPES
 HSV doesn’t always cause symptoms.
 Any symptoms you do notice, and their severity, will generally depend on whether you’re experiencing a primary or recurrent infection.
Primary HSV symptoms
 Symptoms of a primary infection, or first episode, will generally appear anywhere from a few days to a few weeks Trusted Source after exposure
to the virus.
 Primary episodes often include flu-like symptoms, such as:
 fever
 swollen lymph nodes
 body aches and pains, including headache
 unusual tiredness or fatigue
 lack of appetite
 shooting pain at the site of the infection
 You may notice some tingling, burning, or itching at the site of the infection before small, painful blisters appear. There could be one blister or a
small cluster. These blisters will eventually burst and crust over before they begin to heal.
 The blisters that develop during a primary infection may take up to 6 weeks Trusted Source to fully heal. These blisters can still transmit the virus
until they’ve healed completely.
 Sores often itch, and genital sores may cause pain during urination.
 RECURRENT SYMPTOMS
 Some people who live with HSV only ever have one episode, while others continue to have occasional
episodes every several months or so.
 Since your body begins to produce antibodies for the virus, recurrent episodes often become less frequent
with time. They also tend to involve less severe symptoms that improve more rapidly:
 Blisters that appear during a recurrent episode may completely heal within several days rather than several
weeks.
 Blisters may be less noticeable or painful during recurrent episodes.
 If you’ve had a few episodes, you may begin to notice early signs at the site of the infection. These signs,
which generally show up a few hours or days before blisters appear, can include:
1. pain
2. itching
3. burning
4. tingling
 Taking antiviral medication as soon as you notice symptoms could help prevent or shorten the episode —
more on that below.
 DIAGNOSIS OF HERPES

 Cytomegalovirus retinitis is diagnosed clinically.

 Diagnosis of all other herpesvirus infection relies on isolation of the virus through culturing and/or on
detection of viral genes or gene products, particularly using polymerase chain reaction technology.

 A doctor or clinician can diagnose HSV by examining the blisters, flu-like symptoms and early signs, like
tingling or burning.
 Culture; swabbing fluid from the sore and sending it to a laboratory for testing.
 Blood test can determine whether you have HSV antibodies.

NB; You can also test yourself for HSV antibodies with an at-home testing kit. 
 PREVENTION AND TREATMENT OF HERPES
Experts have yet to find a cure for herpes. But various treatments can help relieve your symptoms.
Treatment for HSV includes the following.

 Blisters typically improve on their own, without medical treatment. But if you experience severe or frequent
outbreaks, a doctor or clinician can prescribe antiviral medications. Antivirals can help reduce the number of
episodes you experience and ease the severity of your symptoms.
 Infections with herpes simplex virus 1 and 2 and varicella-zoster virus are currently the most amenable to
therapy; acyclovir, valaciclovir and famciclovir are all licensed therapeutics. Ganciclovir is used to treat
cytomegalovirus retinitis. B virus appears to respond to either of these drugs. There is as yet no treatment for
Epstein-Barr virus or human herpesvirus 6,7 or 8 infections.

Antiviral medications can also help lower your chances of transmitting the virus during an episode or shedding it
when you don’t have symptoms.
Note: There’s no evidence to suggest taking antivirals will lower your chances of contracting the virus if
you don’t have HSV.
These medications generally come in the form of pills and creams. Your doctor or clinician may also recommend an
injection of medication to treat severe symptoms.
Prevention: 

 A vaccine to prevent varicella-zoster virus infections was recently

licensed in the United States.
 Vaccines against herpes simplex virus 2, and cytomegalovirus are
undergoing extensive evaluations in field trials.
 Passive immunization with immunoglobulin or hyperimmune
globulin is used either to prevent infection or as an adjunct to
antiviral therapy.
 HOME REMEDIES

 Plenty of home remedies can help ease pain and discomfort associated with herpes blisters.
 To get relief, try applying the following to sores:
a) a warm or cold compress
b) a paste of baking soda or cornstarch and water
c) a mixture of crushed garlic Trusted Source and olive oil
d) aloe vera Trusted Source
e) tea tree, eucalyptus, or peppermint oil Trusted Source (always dilute with a carrier oil first)
 Some research suggests taking a daily supplement of lysine could also help prevent herpes episodes.
Dosage estimates vary, but taking between 1 and 3 grams of lysine daily appears to have benefit for
managing symptoms and reducing recurrent episodes.
 COMPLICATIONS OF HERPES
 Potential complications
 Once you acquire HSV, the virus lives in your nerve cells permanently. It mostly remains dormant, but it
can reactivate from time to time and cause symptoms.
 For some people, certain triggers can lead to an episode, such as:
 stress
 menstrual periods
 fever or illness
 sun exposure or sunburn
 That said, the virus can cause complications for certain groups of people, including:
 newborns
 immunocompromised people
 people living with chronic health conditions, like cancer or HIV
It’s also possible to develop herpes in the eyes. This condition, known as herpes
keratitis, can develop if you touch a herpes sore and then touch your eye.
Symptoms of herpes keratitis include:
eye pain and redness
discharge or excess tears in the eye
blurred vision
sensitivity to light
a gritty feeling in the eye
 CLASSIFICATION
General Biology of Human Herpesviruses
There are more than 100 known herpesviruses but 8 of them are routinely known to infect only humans:
1. herpes simplex virus types 1 and 2
2. varicella-zoster virus
3. Cytomegalovirus
4. Epstein-Barr virus
5. human herpesvirus 6 (variants A and B)
6. human herpesvirus 7
7. Kaposi's sarcoma virus or human herpesvirus 8.
8. B virus, (A simian virus ) occasionally infects humans.
NB;
All herpesviruses can establish latent infection within specific tissues, which are characteristic for each
virus.
Classification Of herpes viruses

Herpesviruses are divided into three groups:

A. The α herpesviruses
 herpes simplex virus types 1 and 2, and varicella-
zoster virus
 Have a short replicative cycle
 Induce cytopathology in monolayer cell cultures
 Have a broad host range; the ability to replicate in a
wide variety of host tissues.
 Prompt destruction of the host cell .
This sub-family consists of herpes simplex virus 1 and 2
and varicella-zoster virus.
B. β herpesviruses
They include
Human herpesviruses 6 and 7
Have long replicative cycle and restricted host range
Their reproductive life cycle is long (days), with infection
progressing slowly in cell culture systems.
A characteristic of these viruses is their ability to form enlarged
cells, as exemplified by human cytomegalovirus infection.
 These viruses can establish latent infection in secretory glands,
cells of the reticuloendothelial system, and the kidneys
C. γ herpesviruses
They include;
 Epstein-Barr virus
 Human herpesvirus 8
 Have a very restricted host range.

 They replicate in lymphoblastoid cells in vitro and can cause lytic infections in certain
targeted cells.
 Latent virus has been demonstrated in lymphoid tissue. Epstein-Barr virus is a member
of this sub-family. In addition, human herpesvirus 6 and 7 are probably best classified as
a gamma herpesvirus.
 However, the latter has host range properties of the beta sub-family. Further studies will
need to clarify the most appropriate classification of this virus. Kaposi's sarcoma
herpesvirus is most closely related genetically to Epstein-Barr virus.
 MULTIPLICATION OF HERPES
 Multi[plication of herpes occurs by Transcription, genome replication, and capsid
assembly which occur in the host cell nucleus.
 Genes are replicated in a specific order:
1) (1) immediate-early genes, which encode regulatory proteins;
2) (2) early genes, which encode enzymes for replicating viral DNA;
3) (3) late genes, which encode structural proteins.

The tegument and envelope are acquired as the virion buds out through the nuclear
membrane or endoplasmic reticulum. Virions are transported to the cell membrane via
the Golgi complex, and the host cell dies as mature virions are released. Alternatively, in
selected cell types, the virus may be maintained in a latent state. The latent viral genome
may reactivate at any time; the mechanism of reactivation is not known.
Replication process

Replication of all herpesviruses is a multi-step process.

a) Following the onset of infection, DNA is uncoated and transported to the nucleus of the host
cell.
b) This is followed by transcription of immediate-early genes, which encode for the regulatory
proteins.
c) Expression of immediate-early gene products is followed by the expression of proteins
encoded by early and then late genes.
d) Assembly of the viral core and capsid takes place within the nucleus.
e) This is followed by envelopment at the nuclear membrane and transport out of the nucleus
through the endoplasmic reticulum and the Golgi apparatus. Glycosylation of the viral
membrane occurs in the Golgi apparatus.
f) Mature virions are transported to the outer membrane of the host cell inside vesicles.
g) Release of progeny virus is accompanied by cell death. Replication for all herpesviruses is
considered inefficient, with a high ratio of non-infectious to infectious viral particles .
Latency
 Each virus within the family has the potential to establish latency in specific host cells
 the latent viral genome may be either extra-chromosomal or integrated into host cell DNA.
 Herpes simplex virus 1 and 2 and varicella-zoster virus all establish latency in the dorsal root
ganglia.
 Epstein-Barr virus can maintain latency within B lymphocytes and salivary glands.
 Cytomegalovirus, human herpesvirus 6 and 7, Kaposi's sarcoma herpesvirus and B virus have
unknown sites of latency.
 Latent virus may be reactivated and enter a replicative cycle at any point in time.
 The reactivation of latent virus is a well-recognized biologic phenomenon, but not one that is
understood from a biochemical or genetic standpoint. It should be noted here that an anti-
sense message to one of the immediate-early genes (alpha-O) may be involved in the
maintenance of latent virus.
 Stimuli that have been observed to be associated with the reactivation of latent herpes
simplex virus have included stress, menstruation, and exposure to ultraviolet light.
Pathogenesis
 A critical factor for transmission of herpes simplex viruses, regardless of virus type, is the
requirement for intimate contact between a person who is shedding virus and a susceptible
host.
 After inoculation onto the skin or mucous membrane and an incubation period of four to six
days, herpes simplex virus replicates in epithelial cells
 As replication continues, cell lysis and local inflammation ensue, resulting in characteristic
vesicles on an erythematous base. Regional lymphatics and lymph nodes become involved:
viremia and visceral dissemination may develop depending upon the immunologic
competence of the host.
 In all hosts, the virus generally ascends the peripheral sensory nerves to reach the dorsal root
ganglia.
 Replication of herpes simplex virus within neural tissue is followed by retrograde axonal
spread of the virus back to other mucosal and skin surfaces via the peripheral sensory nerves.
 Virus replicates further in epithelial cells, reproducing the lesions of the initial infection, until
infection is contained through both systemic and mucosal immunity.
 HOST DEFENSES

 Interferon and humoral, mucosal, and cellular

immunity are important defenses.
 Herpes simplex virus infections are more severe
in immunocompromised hosts.
EPIDEMIOLOGY

 Herpes simplex virus 1 transmission is primarily

oral
 Herpes simplex virus 2 primarily genital.
 Transmission requires intimate contact.
KNOWN HERPES VIRUSES
1. Varicella-Zoster Virus
Clinical Manifestations

Primary varicella-zoster virus infection causes varicella (chickenpox).

Reactivation of latent virus (usually in adults) causes herpes zoster (shingles),
manifesting as vesicular rash with a dermatomal distribution and acute neuritis.
Pathogenesis
 Varicella-zoster virus is usually transmitted by droplets and
replicates initially in the nasopharynx.
 In seronegative individuals, viremia and chickenpox ensue.
 Latency is established in dorsal root ganglia, and virus reactivation
results in virion transport down sensory nerves.
.

Epidemiology
Varicella-zoster virus is highly contagious; about 95 percent of adults show
serologic evidence of infection.
2. Cytomegalovirus
Clinical Manifestations
Cytomegalovirus causes three clinical syndromes.
1. Congenital cytomegalovirus infection (when symptomatic) causes
hepatosplenomegaly, retinitis, rash, and central nervous system
involvement.
2. In about 10 per cent of older children and adults, primary cytomegalovirus
infection causes a mononucleosis syndrome with fever, malaise, atypical
lymphocytosis, and pharyngitis.
3. Immunocompromised hosts (transplant recipients and human
immunodeficiency virus [HIV]-infected individuals) may develop life-
threatening disseminated disease involving the lungs, gastrointestinal tract,
liver, retina, and central nervous system.
Pathogenesis
Cytomegalovirus replicates mainly in the salivary glands and kidneys and is
shed in saliva and urine. Replication is slow, and the virus induces
characteristic giant cells with intranuclear inclusions.

Epidemiology
Transmission is via intimate contact with infected secretions.
Cytomegalovirus infections are among the most prevalent viral
infections worldwide.
3. Epstein-Barr Virus
Clinical Manifestations
Epstein-Barr virus causes classic mononucleosis.
In immunocompromised hosts, the virus causes a
lymphoproliferative syndrome.
In some families, Epstein Barr virus causes
Duncan's syndrome.
Pathogenesis

Epstein Barr virus replicates the epithelial cells of the oropharynx

and in β lymphocytes
.

Epidemiology

Epstein Barr virus is transmitted by intimate contact, particularly

via the exchange of saliva.
4. Human Herpesvirus 6 and 7
Clinical Manifestations
Human herpes viruses 6 and 7 are associated with exanthem
subitem (roseola) and with rejection of transplanted kidneys.
Pathogenesis

The pathogenesis is poorly understood.

Epidemiology

Antibodies to this virus are present in almost everyone by age 5

5. Human Herpesvirus 8
Clinical Manifestations
Human herpesvirus 8 has been found associated with
Kaposi's sarcoma in AIDS patients as well as intra-
abdominal solid tumors.

Pathogenesis and Epidemiology

Virtually nothing is known about the pathogenesis and
epidemiology of this newly described herpesvirus.
6. B Virus

Clinical Manifestations
In humans, B virus causes an encephalitis that is usually fatal; survivors
have brain damage.
Pathogenesis
B virus is transmitted to humans by the bite of infected rhesus monkeys and
is transported up neurons to the brain.
Epidemiology
The reservoir for the disease is latent infection in rhesus
monkeys, particularly those from Southeast Asia and India.
In stressed or unhealthy animals, the virus may reactivate
and appear in saliva
CLINICAL MANIFESTATIONS OF HSV-1 AND
HSV-2