Latest research on Tenofovir

Tenofovir disoproxil fumarate (a prodrug of tenofovir), marketed by Gilead Sciences under the trade name Viread®, belongs to a class of antiretroviral drugs known as nucleotide analogue reverse transcriptase inhibitors (nRTIs), which block reverse transcriptase, an enzyme crucial to viral production in HIV-infected people. [Wikipedia] In vivo tenofovir disoproxil fumarate is converted to tenofovir, an acyclic nucleoside phosphonate (nucleotide) analog of adenosine 5'-monophosphate.

Latest findings

Preliminary tests showed that these dosages give roughly similar intracellular concentrations of the active drug (Tenofovir diphosphate) as measured in the vagina after Tenofovir 1% gel use (not shown) (Hendrix et al., 2013). [source]
In the epithelial cells, Tenofovir did not significantly change chemokine, chemokine receptor, and cluster of differentiation (CD) genes, and it suppressed ISG 15 (interferon-stimulated gene 15) and MX1 (myxovirus resistance 1), which were induced in the biopsies. [source]
The number of genes affected was initially higher with 500 μM than with 50 μM Tenofovir, but equalized after 14 days of culture (Figure 4A). [source]
Next, we confirmed the expression changes of select genes by ddPCR with vaginal epithelial cells from four healthy women: mRNA copies of DSP (desmoplakin) and IL-10 significantly decreased, and KIAA0101 significantly increased during 7 days of Tenofovir treatment, as seen in the microarray data (Figure 4B). [source]
In fact, IL-10 transcripts were virtually eliminated at 7 days (p = 0.002 and p = 0.003 for 50 and 500 μM, respectively), and KIAA0101 increased more than 10-fold at 500 μM Tenofovir (p = 0.005). [source]
Tenofovir treatment of primary vaginal epithelial cells in vitro mostly impacted the same biological processes as it did in the rectum in vivo (Figure 4D and Figure 3—figure supplement 2). [source]
Furthermore, Tenofovir enhanced vaginal epithelial cell proliferation and/or cell survival in vitro (p = 0.02) (Figure 4E). [source]
Our microarray results indicated that Tenofovir suppresses PNPT1 (Figure 1C), which has been characterized as a master regulator of RNA import into mitochondria and whose deletion impairs mitochondrial function (Wang et al., 2010). [source]
To directly assess mitochondrial function, we picked one of the 13 genes encoded by mitochondrial DNA, ATP synthase F0 subunit 6 (ATP6), a key component of the proton channel (Houstek et al., 2006), and measured its transcription by RT-ddPCR in the 9 cm biopsies of all 15 study participants in the Tenofovir arm (Figure 5B). [source]
Next, we evaluated changes in mitochondrial number and size between baseline and after 7 days of treatment in two study participants chosen for exhibiting pronounced PNPT1 suppression by Tenofovir. [source]