Table 1.

Main data on herpes simplex virus type 1 (HSV1) and AD from the author’s laboratory between 1991 and 2015.

Discovery	Reference
HSV1 DNA detected (by PCR) in brains of elderly controls and AD patients.	Jamieson et al. (1991)
HSV1 in brain of APOE-ε4 carriers confers high risk of AD. APOE-e4 is a risk for cold sores. First of several articles showing that APOE genotype modulates extent of microbial damage.	Itzhaki et al. (1997)
HHV6 DNA is present in AD brains.	Lin et al. (2002)
Intrathecal antibodies to HSV1 found in the elderly, showing that productive infection of HSV1 in brain has occurred.	Wozniak et al. (2005)
Aβ accumulation occurs in HSV1-infected cell cultures.	Wozniak et al. (2007)
HSV1 DNA is located specifically in amyloid plaques of AD brains.	Wozniak et al. (2009b)
AD-like tau (P-tau) accumulation occurs in HSV1-infected cell cultures.	Wozniak et al. (2009a)
HSV1 activates BACE1 via activation of PKR, then phosphorylation of eIF2-α.	Ill-Raga et al. (2011)
Acyclovir and other HSV1 replication-inhibitors reduce greatly the levels of Aβ and P-tau in HSV1-infected cell cultures.	Wozniak et al. (2011)
IVIG reduces greatly the levels of Aβ and P-tau in HSV1-infected cell cultures.	Wozniak and Itzhaki (2013)
Helicase primase inhibitor reduces greatly the levels of Aβ and P-tau in HSV1-infected cell cultures.	Wozniak et al. (2013)
Fucan reduces greatly the levels of Aβ and P-tau in HSV1-infected cell cultures.	Wozniak et al. (2015)
Interpretation of Taiwan population epidemiological data on HSV and risk of AD and antiherpes effects on development of senile dementia.	Itzhaki and Lathe (2018)