Herpes simplex virus 1 and 2, also known by their taxonomic names Human alphaherpesvirus 1 and Human alphaherpesvirus 2, are two members of the human Herpesviridae family, a set of viruses that produce viral infections in the majority of humans. Both HSV-1 and HSV-2 are very common and contagious.

1. Herpes Simplex
Virus 1 & 2
Name: Odeyemi Aduragbemi Noah

2. Herpes simplex virus (HSV) is a member of the
Alphaherpesvirinae subfamily of the Herpesviridae family.
HSV is a double-stranded DNA virus that infects a variety
of host tissues and is characterized by a lytic and latent
cycle.
What is Herpes?
According to estimates from the World Health Organization
Trusted 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

3. HERPES Viruses structure
 A core containing the large double-stranded
DNA genome
 Genome is 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
Herpesviruses have a unique four-layered structure:

4. Viral Replication
 Upon entry into the host cell nucleus, three
distinct phases of gene transcription and protein
synthesis are initiated producing the immediate-
early, early, and late proteins
 Viral nucleocapsid assembly occurs within the
host cell nucleus.
 The virus acquires its final envelope by budding
into cytoplasmic vesicles

5. Herpes Simplex Virus
 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.
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.

6. Features of herpes simplex?
HSV type 1 (HSV-1) and type 2 (HSV-2) are distinguished by two main criteria:
antigenicity and location of lesions. Lesions caused by
• HSV-1 are, in general, above the waist
• HSV-2 are below the waist.
Diseases
 HSV-1 causes acute gingivostomatitis, recurrent herpes labialis (cold sores),
keratoconjunctivitis (keratitis), and encephalitis, primarily in adults.
 HSV-2 causes herpes genitalis (genital herpes), neonatal encephalitis and other forms
of neonatal herpes, and aseptic meningitis. Infection by HSV-1 or HSV-2 is a common
cause of erythema multiforme.

7. Herpes simplex virus 1

8. Herpes simplex virus 2

10. Summary of Replicative Cycle
 The cycle begins when HSV-1 binds first to heparan sulfate on the cell surface and
then to a second receptor, nectin.
 Fusion of the viral envelope with the cell membrane, the nucleocapsid and the
tegument proteins are released into the cytoplasm.
 The viral nucleocapsid is transported to the nucleus, where it docks to a nuclear
pore and the genome DNA enters the nucleus along with tegument protein VP16.
 The linear genome DNA now becomes circular. VP16 interacts with cellular
transcription factors to activate transcription of viral immediate early (IE) genes by
host cell RNA polymerase.
 IE mRNA is translated into IE proteins that regulate the synthesis of early proteins
such as the DNA polymerase that replicates

12. Pathogenesis & Immunity
1. The virus replicates in the skin or mucous
membrane at the initial site of infection.
2. Migrates up the neuron by retrograde axonal flow
and becomes latent in the sensory ganglion cells.
3. HSV-1 becomes latent in the trigeminal ganglia,
whereas HSV-2 becomes latent in the lumbar and
sacral ganglia.
4. The virus can be reactivated from the latent state by
a variety of inducers (e.g., sunlight, hormonal
changes, trauma, stress, and fever), at which time it
migrates down the neuron and replicates in the skin,
causing lesions.

13. Laboratory Diagnosis
1. An important diagnostic procedure is isolation of
the virus from the lesion by growth in cell culture.
2. ELISAs Detecting virus-specific glycoproteins in
enzyme-linked immunosorbent assays .
3. A rapid diagnosis from skin lesions can be made by
using the Tzanck smear, in which cells from the
base of the vesicle are stained with Giemsa stain.
4. PCR A rapid diagnosis of encephalitis can be
made by detecting HSV-1 DNA in the spinal fluid by
using a PCR assay, but virus is rarely recovered
from the spinal fluid.
5. Serologic tests

14. Treatment
 Acyclovir, PO, IV, topical
 Penciclovir topical
 Famciclovir PO
 Valacyclovir PO
In summary, these medications intercept HSV infections by inhibiting viral DNA synthesis
through various mechanisms, including competitive inhibition of viral DNA polymerase
and chain termination. They are effective in reducing the severity and duration of
symptoms during outbreaks, as well as in preventing recurrent episodes when taken
regularly as suppressive therapy.

15. Reference
1. Gruter W (1924) Das herpesvirus, seine atiologische und klinische bedeutung. Munch
Med Wschr 71:1058
2. Smith G (2012) Herpesvirus transport to the nervous system and back again. Annu Rev
Microbiol 66:153–176
3. Gupta R, Warren T, Wald A (2007) Genital herpes. Lancet 370(9605):2127–2137
4. Anderson BJ (2003) The epidemiology and clinical analysis of several outbreaks of
herpes gladiatorum. Med Sci Sports Exerc 35(11):1809–1814