Cold sores : Introduction, Entry, Symptoms, Diagnosis and Cure

Cold Sores: Introduction, Entry, Symptoms, Diagnosis and Cure

Introduction of cold sores

The term herpes is derived from the Greek word meaning “to creep:’ Clinical descriptions of herpes lesions date back to the time of Hippocrates (circa 400 BCE). Herpes lesions are caused by the double-stranded DNA viruses commonly called herpes simplex viruses (genus Simplexvirus). Herpes simplex viruses have icosahedral capsids and are enveloped. The genome encodes approximately 100 proteins.

Entry of herpesvirus into host

  • The herpesvirus genome must first enter an epithelial cell for the initiation of infection. Transmission is through direct contact of epithelial tissue surfaces with the virus.
  • Herpes simplex virus type 1 (HSV-1; species Human herpesvirus 1) was initially thought to infect oral mucosal epithelium to cause cold sores or fever blisters, and herpes simplex virus type 2 (HSV-2; species Human herpesvirus 2) was thought to infect genital epithelium to cause genital herpes.
  • The initial association is between proteoglycans of the epithelial cell surface and viral glycoproteins. This is followed by a specific interaction with one of several cellular receptors collectively termed HVEMs for herpesvirus entry mediators.
  • The capsid, along with some associated proteins, then migrates along the cellular microtubule transport machinery to nuclear envelope pores. This “docking” is thought to result in the viral DNA being injected through the nuclear envelope pores while the capsid remains in the cytoplasm.

Effects of herpesvirus within an infected host

  • Active and latent phases have been identified within an infected host. After an incubation period of about a week, the active phase begins.
  • During the active phase, the virus multiplies explosively; between 50,000 and 200,000 new virions are produced from each infected cell.
  • During this replication cycle, herpesvirus inhibits its host cell’s metabolism and degrades host DNA, inducing apoptosis. As a result, the cell dies, releasing viral progeny to infect other cells. Such an active infection may be symptom free, or painful blisters in the infected tissue may occur.
  • Healthy people can transmit HSV to other hosts or their newborns. This is especially true of transmission with HSV-2; it can be passed to sexual contacts even when there are no clinical signs of infection.
  • Blisters involving the epidermis and surface mucous membranes of the lips, mouth, and gums (gingivostomatitis) are referred to as herpes labialis.
Herpes simplex fever blisters on the lip, caused by herpes simplex type 1 virus

Symptoms of HSV infections

  • Primary and recurring HSV infections also may occur in the eyes, causing herpetic keratitis (inflammation of the cornea) currently a major cause of blindness in the United States.
  • Blisters involving the epidermis and surface mucous membranes of the genitals and perianal region are referred to as genital herpes.
  • In all cases, the blisters are the result of cell lysis and the development of a local inflammatory response; they contain fluid and infectious virions.
  • Fever, headache, muscle aches and pains, a burning sensation, and general soreness are frequently present during the active phase.

Virulence factor of Herpes simplex virus

  • Although blisters usually heal within a week, after a primary infection, a very interesting virulence factor initiates the long-term survival of HSV-1 -infected neurons, inducing the latent phase of infection.
  • As the active infection is curtailed by a vigorous cellular immune response, virus released from infected oral epithelia travels to the trigeminal nerve ganglion.
  • The retreat to the nerve ganglion (cells) results in a latent state for the lifetime of the infected host, apparently to prevent further detection by the host immune system.
  • With time, however, HSV -1 occasionally emerges from latency to grow productively, potentially attracting the wrath of the immune system.
  • Stressful stimuli such as excessive sunlight, fever, trauma, chilling, emotional stress, and hormonal changes can reactivate the virus. Once reactivated, the virus moves from the nerve ganglion down a peripheral nerve and back to epithelial cells to produce the active phase. Interestingly, not all infected neurons die from a productive infection. Latently infected neurons and some neurons with productive HSV infection survive.
  • How is this? It turns out that a small HSV gene has been identified that can protect the infected neuron from host immune cells. The gene encodes the latency associated transcript, or LAT, an 8.5-kb RNA. LAT is spliced as an mRNA precursor, but no consistently expressed protein has been found to be translated from it.
  • Instead, a long-lived 2-kb microRNA (miR-LAT ) remaining in the nucleus appears to promote degradation of two proteins that inhibit cell proliferation and initiate apoptosis. In other words, miR-LAT prevents the infected cell from self-destruction, ensures neuron survival, and provides a hiding place for the virus.

Cure of cold sores

  • The drugs vidarabine and acyclovir are effective against cold sores.
  • Idoxuridine and trifluridine are used to treat herpes infections of the eye.
  • By adulthood, 70 to 90% of all people in the United States have been infected and have type 1 herpes antibodies.

Diagnosis of HSV-1 infection

  • Diagnosis of HSV-1 infection is by ELISA and direct fluorescent antibody screening of tissue.
  • Diagnosis may also be made through the recovery of viral DNA by PCR. These tests are especially useful in individuals who are particularly susceptible to severe infections.

Reference and Sources

  • https://ppdictionary.com/viruses/hsv.htm
  • http://whale.to/cancer/consider_the_lilies.html
  • https://www.cram.com/flashcards/nbde-released-microbiology-pathology-5373605
  • https://quizlet.com/87500157/quiz-18-chapter-38-flash-cards/
  • https://ufdc.ufl.edu/UFE0041034/00001
  • https://quizlet.com/45501136/drury-microbiology-208-test-4-flash-cards/
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC111616/

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