E-Book 2nd Congress

  • The Functional Effect of Herpes Simplex Virus (HSV) on Alzheimer's Disease Approach: A Review Study
  • Saba Ebrahimi Baghbani,1 Ali Ahmadi,2,*
    1. MD. Student, Department of Medicine, Faculty of Medical Sciences, Islamic Azad University Sari Branch, Sari, Iran
    2. M.Sc. Student, Department of Genetics, Faculty of Advanced Technologies and Sciences in Medicine, Islamic Azad University Tehran Medical Science, Tehran, Iran


  • Introduction: Alzheimer's disease is a neurodegenerative disorder in which progressive decline in cognitive function leads to memory loss and Dementia. In this disease, the limbic system and the structures of the cerebral cortex, especially the temporal lobe, are destroyed. In recent years, it was estimated that 35.5 million people worldwide have Dementia, and this number is projected to reach 65.7 million in 2030 and 115.4 million in 2050. The 2010 Alzheimer's World Report estimated dementia costs 604 billion U.S. dollars in 2010. Most cases of Alzheimer's disease are sporadic, and a small proportion of them are hereditary, called familial Alzheimer's disease. The main risk factor for Alzheimer's disease is aging. Different factors can cause Alzheimer's disease. Among the genetic factors of type 4 allele, Apolipoprotein E gene is very well known among environmental factors chronic brain infections have an effective role in the pathogenesis of Alzheimer's disease. Among the various factors associated with the pathogenesis of Alzheimer's disease (AD), more attention should be paid to the role of pathogens. Epidemiological and experimental evidence suggests that recurrent infections with herpes simplex virus type 1 can be a risk factor for Alzheimer’s disease, but its functional and molecular mechanisms have not yet been fully identified. Multifactorial counties such as Alzheimer's are important to determine the role of different factors causing the disease and its related mechanisms.
  • Methods: This study is an interventional study with narrative review approach that was conducted in 2022 by searching keywords such as HSV, Dementia, Alzheimer and Apolipoproteins in valid databases such as Science Direct, PubMed, Scopus. Finally, 15 articles were reviewed, of which 10 were included in the study.
  • Results: According to studies from the papers, the results are that the risk of Alzheimer's disease with HSV1 in the brain increases by 3.1 times and this risk increases 7.2 times in simultaneous HSV1/APOE4 carriers compared to the control group. Herpes simplex virus type 1 is a pandemic that infects more than 80 percent of people over the age of 65 worldwide. HSV1 is a neurotropic virus with distant DNA that initially infects the epithelial cells of the nasal mucosa and mouth. New viral components that develop can enter sensory neurons and transmit their exons to trigeminal ganglions, causing a latent infection. The virus is periodically activated and causes herpes blisters. However, trigeminal ganglion bipolar neurons are also drawn to the trigeminal nuclei located in the brainstem. Neurons are drawn from these nuclei to the thalamus and finally the sensory cortex. This is the pathway through which the activated virus can reach the central nervous system (CNS) and cause acute neuronal disorders such as HSE (Herpes Simplex Encephalitis) or a minor asymptomatic infection or a lifelong latent infection, aging with weakening of the immune system can exacerbate the occurrence of this condition, in addition to the neuronal pathway, HSV-1 can also enter the central nervous system through the bloodstream, chronic infection HSV_1 It causes continuous activation of microglia, which is caused by antiviral induction of neurotoxic agents at the same time, then ATP and MMP3 released from damaged neurons further activate the microglia, with chronic activation of microglia caused by HSV1 infection, creating a faulty cycle and paving the way for the creation of a stronger Alzheimer's. Activation of HSV_1 lytic cycles in the brain is commonly associated with stress and suppression of the immune system and inflammation
  • Conclusion: Dioxin responsive elements (DRE) are potentially numerous active in the regulatory regions of viral genes. In the five HSV1 genes these DREs are found in the observed monitoring areas of dioxin, a key member of the HSV1 activator complex, in brain tissue and may be associated with glial cells instead of neurons.
  • Keywords: HSV, Dementia, Alzheimer, Apolipoproteins