Cold sores are caused by certain strains of the herpes simplex virus (HSV). HSV-1 usually causes cold sores. HSV-2 is usually responsible for genital herpes. However, either type can cause sores in the facial area or on the genitals. Most people who are infected with the virus that causes cold sores never develop signs and symptoms. The herpes simplex virus usually enters the body through a break in the skin around or inside the mouth. It is usually spread when a person touches a cold sore or touches infected fluid-such as from sharing eating utensils or razors, kissing an infected person, or touching that person's saliva. A parent who has a cold sore often spreads the infection to his or her child in this way. Cold sores can also be spread to other areas of the body. Herpes simplex virus type 1 (HSV-1) is a ubiquitous human pathogen. While there has been extensive research into the evolutionary relationships among herpesviruses, there is little data on the evolutionary relationship of HSV-1 based on sequence analysis of clinical isolates. The present study aims to be the first to document the molecular epidemiology and genetic diversity and frequency of recombination of HSV-1 (n = 42) clinical isolates in Ireland. The entire 1,171 bp of the gI-1 gene and 717 bp of the gG-1 gene of 42 clinical Irish isolates were amplified, sequenced and the phylogenies reconstructed. Putative recombinants were examined using bootscan analysis. Phylogenetic reconstruction of the nucleotide sequence alignments of the entire genes of amplified glycoproteins gI and gG suggested that three distinct HSV-1 genogroups were circulating in the Irish population. At least 15 HSV-1 intergenic recombinants with a recombination point between gI and gG, and 11 HSV-1 intragenic recombinants were detected. There was no evident association between genetic group and gender, disease recurrence or anatomical site of infection. Genital isolates (n = 30) belonged to all genogroups. However, two HSV-1 isolates, Irl 31 and Irl32, from a patient with severe mucocutaneous infection nonresponsive to acyclovir and isolated over a prolonged period were both intragenic and intergenic recombinants. The detection of variability and recombination in gG and gI genes of both HSV-1 may provide a mechanism to evade the host immune response thereby maintaining the viral genome. The variability and recombination detected may also have implications for the detection, diagnosis and treatment of HSV. Cold sores usually clear up without treatment within 7 to 10 days.
Antiviral tablets or cream can be used to ease your symptoms and speed up the healing time. Antiviral creams such as aciclovir or penciclovir (also known as Fenistil) may speed up the healing time of a recurrent cold sore infection if used correctly.Cold sore creams are widely available over the counter from pharmacies without a prescription. They are only effective if you apply them as soon as the first signs of a cold sore appear, when the herpes simplex virus is spreading and replicating. Using an antiviral cream after this initial period is unlikely to have much effect. Cold sore patches that contain a special gel called hydrocolloid are also available. They are an effective treatment for skin wounds and are placed over the cold sore to hide the sore area while it heals Various vaccine candidates have been developed, the first ones in the 1920s, but none has been successful to date. Due to the genetic similarity of both herpes simplex virus types (HSV-1 and HSV-2), the development of a prophylactic-therapeutic vaccine which is proven effective against one type of the virus would provide fundamentals for vaccine-development for the other virus type. As of 2015, several vaccine candidates are in different stages of clinical trials as they are being tested for safety and efficacy, including at least three vaccine candidates in the US and one in Australia.