Seyyede Nafise Vakili - Department of Virology, Faculty of Medicine, Shiraz University, Shiraz, Iran
Mohamadreza Diba - Department of Biochemistry, Faculty of Medicine, Shiraz University, Shiraz, Iran
Zahra Meshkat - Department of Microbiology and Virology, Faculty of Medicine, Mashhad University, Mashhad, Iran

Many studies were demonstrated that chronic bacterial and viral infections as possible risk factors for neurodegenerative diseases, includingParkinson’s disease, amyotrophic lateral sclerosis and Alzheimer’s disease. Infections of the central nervous system may produce multiple damages in infected and neighbouring normal cells. The activation of immune responses and inflammatory processes cause chronicdamage resulting in alterations of neuronal function and viability. Viral agents have been reported to produce and deposit of molecular hallmarks of neurodegeneration, such as misfolded protein aggregates, oxidative stress, deficient autophagic processes, synaptopathies andneuronal death. Also, these effects may act in synergy with other risk factors, such as aging, concomitant metabolic diseases and the host’s specific genetic signature in patients. Much evidence demonstrates that pathogens directly and indirectly induced Alzheimer’s disease pathology, including amyloid accumulation, phosphorylation of tau protein, neuronal injury, and apoptosis. Many studied were showed that herpes simplex virus type 1 (HSV1-) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1- in the brain of carriers of the type 4 alleles of the apolipoprotein E gene is reactivated by different events such as immunosuppression, peripheral infection,and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD. Also, Human herpesvirus type 6 (HHV6-) is another virus investigated as a potential contributor to Alzheimer’s disease. However, it is uncertain whether its presence and activity is a cause or a consequence of the disease and it may be that HHV6- merely exacerbates the potentially harmful effects of HSV1- in patients. Conclusion: This review will focus on the role of HSV- 1 and HHV-6 in Alzheimer›s disease progression.