Treatment
Similar to other herpesviridae, the herpes simplex viruses establish latent lifelong infection, and thus cannot be eradicated from the body with current treatments.Treatment usually involves general-purpose antiviral drugs that interfere with viral replication, reduce the physical severity of outbreak-associated lesions, and lower the chance of transmission to others. Studies of vulnerable patient populations have indicated that daily use of antivirals such as aciclovir and valaciclovir can reduce reactivation rates. The extensive use of antiherpetic drugs has led to the development of some drug resistance, which in turn may lead to treatment failure. Therefore, new sources of drugs are broadly investigated to address the problem. In January 2020, a comprehensive review article was published that demonstrated the effectiveness of natural products as promising anti-HSV drugs. Pyrithione, a zinc ionophore, has shown antiviral activity against herpes simplex. Alzheimers disease
In 1979, it was reported that there is a possible link between HSV-1 and Alzheimers disease, in people with the epsilon4 allele of the gene APOE. HSV-1 appears to be particularly damaging to the nervous system and increases ones risk of developing Alzheimers disease. The virus interacts with the components and receptors of lipoproteins, which may lead to the development of Alzheimers disease. This research identifies HSVs as the pathogen most clearly linked to the establishment of Alzheimers. According to a study done in 1997, without the presence of the gene allele, HSV-1 does not appear to cause any neurological damage or increase the risk of Alzheimers.
Diagnosis
Talley et al. suggested 3 diagnostic criteria which are still widely used:

the presence of gastrointestinal symptoms,
histological demonstration of eosinophilic infiltration in one or more areas of the gastrointestinal tract or presence of high eosinophil count in ascitic fluid (latter usually indicates subserosal variety),
no evidence of parasitic or extraintestinal disease.Hypereosinophilia, the hallmark of allergic response, may be absent in up to 20% of patients, but hypoalbuminaemia and other abnormalities suggestive of malabsorption may be present. CT scans may show nodular and irregular thickening of the folds in the distal stomach and proximal small bowel, but these findings can also be present in other conditions like Crohns disease and lymphoma.The endoscopic appearance in eosinophilic gastroenteritis is nonspecific; it includes erythematous, friable, nodular, and occasional ulcerative changes. Sometimes diffuse inflammation results in complete loss of villi, involvement of multiple layers, submucosal oedema and fibrosis.Definitive diagnosis involves histological evidence of eosinophilic infiltration in biopsy slides. Microscopy reveals >20 eosinophils per high power field. Infiltration is often patchy, can be missed and laparoscopic full thickness biopsy may be required. Radio isotope scan using technetium (99mTc) exametazime-labeled leukocyte SPECT may be useful in assessing the extent of disease and response to treatment but has little value in diagnosis, as the scan does not help differentiating EG from other causes of inflammation.When eosinophilic gastroenteritis is observed in association with eosinophilic infiltration of other organ systems, the diagnosis of idiopathic hypereosinophilic syndrome should be considered. Management
Corticosteroids are the mainstay of therapy with a 90% response rate in some studies.