Surprisingly, the fermentation broth of Rac12 was confirmed to produce salidroside and DL-AP3 p-tyrosol by HPLC assay in this study. These results suggest that versatile fungal endophytes may produce many novel antioxidant products, including the same bioactive chemicals as those of their hosts. The important relationship between Rac12 and its host can be elucidated by illustrating the biosynthetic pathway in two organisms, and the production from Rac12 will be significantly increased by screening industrial mutants and optimizing the fermentation process in future studies. Accordingly, endophytic fungi were highly abundant in Rhodiola plants. However, their mutual relationship, ecological function, and relevance of metabolic pathways need extensive investigation. These species are potential viable sources for exploring novel natural antioxidant products. Highly active antiretroviral therapy has succeeded in lowering human immunodeficiency virus type 1 levels in most patients, in some cases to undetectable levels. However, this therapy alone cannot completely eradicate the virus. Many studies have shown that this is most likely because of a stable population of latently infected CD4 + T cells, which cannot be elimated by HAART on its own. The small pool of latently infected cells that is present in each infected individual functions as a reservoir for the virus. Because of its slow decay rate, this reservoir is now considered to be the main barrier to viral eradication via current antiretroviral drugs. Much progress has recently been made to elucidate the molecular mechanisms underlying HIV-1 proviral latency, which is intimately tied to HIV-1 transcription level. Several factors contribute to the transcriptional silencing of integrated HIV-1 proviruses. The first is the site of proviral integration into the host cell genome and the cellular chromatin environment at this site. The second mechanism involves the epigenetic silencing by post-transcriptional modifications on histones that are key components of BAY 41-8543 nucleosome and capable to modulate the chromatin structure. The third mechanism involves the ability of host cell factors to restrict HIV-1. Transcription factors such as yin and yang 1 and late SV40 factor repress HIV-1 replication in infected CD4 + T cells by recruiting HDAC1 to the repressor complex sequence located at nucleotides �C10 to +27 in the LTR. Other host transcription factors, such as NF-kB subunit p50 homodimers and C-promoter binding factor 1, can also recruit HDACs to the LTR and inhibit viral transcription similarly to YY1 in several cell lines. The fourth mechanism involves the microRNAs and RNA interference. It has been shown that cellular miRNAs may inhibit HIV-1 gene expression by interfering with histone acetylation.