China approves HIV drug for Covid patients

Into the rabbit hole we go.

So, earlier today a piece of news went viral pretty fast.

China approves Genuine Biotech's HIV drug for COVID patients

BEIJING, July 25 (Reuters) - China on Monday gave conditional approval to domestic firm Genuine Biotech's Azvudine pill to treat certain adult patients with COVID-19, adding another oral treatment option against the coronavirus.

Reporting by Roxanne Liu and Ryan Woo Editing by Louise Heavens and Mark Potter

I would very much like to finish my Kynurenine series, because it directly correlates with this, but alas I rather refer to this one some point in the near future.

Of course, the usual suspects went deep into their erroneous bullshit of “VAIDS” (it is not a thing, whoever pushes this is literally manipulating their followers for something else). But of course, clues for the real reason are always a few seconds away in a quick Google search. First, we need to look into what Azvudine is or does.

Azvudine is a thymus-homing anti-SARS-CoV-2 drug effective in treating COVID-19 patients

Abstract

Azvudine (FNC) is a nucleoside analog that inhibits HIV-1 RNA-dependent RNA polymerase (RdRp). Recently, we discovered FNC an agent against SARS-CoV-2, and have taken it into Phase III trial for COVID-19 patients. FNC monophosphate analog inhibited SARS-CoV-2 and HCoV-OC43 coronavirus with an EC50 between 1.2 and 4.3 μM, depending on viruses or cells, and selective index (SI) in 15–83 range. Oral administration of FNC in rats revealed a substantial thymus-homing feature, with FNC triphosphate (the active form) concentrated in the thymus and peripheral blood mononuclear cells (PBMC). Treating SARS-CoV-2 infected rhesus macaques with FNC (0.07 mg/kg, qd, orally) reduced viral load, recuperated the thymus, improved lymphocyte profiles, alleviated inflammation and organ damage, and lessened ground-glass opacities in chest X-ray. Single-cell sequencing suggested the promotion of thymus function by FNC. A randomized, single-arm clinical trial of FNC on compassionate use (n = 31) showed that oral FNC (5 mg, qd) cured all COVID-19 patients, with 100% viral ribonucleic acid negative conversion in 3.29 ± 2.22 days (range: 1–9 days) and 100% hospital discharge rate in 9.00 ± 4.93 days (range: 2–25 days). The side-effect of FNC is minor and transient dizziness and nausea in 16.12% (5/31) patients. Thus, FNC might cure COVID-19 through its anti-SARS-CoV-2 activity concentrated in the thymus, followed by promoted immunity.

FNC selectively activated through phosphorylation in the thymus in vivo

FNC achieved great success in treating patients suffering from COVID-19 during the SAR-CoV-2 outbreak 2020 in China (see results below); the clinical dose of FNC was 5 mg per day in oral administration, much lower than that of remdesivir (100 mg per day, iv) and favipiravir (1000 mg per day, oral), the efficiency of FNC in treating patients with COVID-19 as a regular viral RdRp inhibitor needed further exploration.

So by the abstract alone, you can superficially understand the drug use, while the main MoA (mode of action, the main use of the drug) is for antiviral purposes against HIV, when it comes to SARS-CoV-2 it does something else entirely. I want you to pay very close attention to the bold part in the first paragraph, don’t worry I will spill some of it here.

The second paragraph is even more intriguing. They have been using this drug since 2020…

The human thymus in the chest is a primary immune organ and the birthplace of circulating T lymphocytes responsible for the host immunity in general. The aging human thymus shrinks significantly, along with the reduced immunity and distorted immune regulation in older adults. In this SARS-CoV-2 pandemic, one of the important abnormalities in the blood is lymphopenia caused by SARS-CoV-2,7,9,35 indicating damage to the immune system. Furthermore, elevated cytokine levels (IL-1β, INF-γ, TNF-α, and IL-6),19,20,21,22,23,24,36 which are also closely related to the function of lymphocytes or monocytes, are critical change in COVID-19 and can cause severe cytokine storm and death.9 Damaged regulatory function in T cells can be an important factor responsible for the abnormal production of cytokines. Indeed, aged patients with COVID-19 have much higher mortality compared with those in middle or young age,5,37 probably because their defensive immunity and regulatory function in lymphocytes or monocytes are injured. FNC treatment in viral (+) monkeys increased the levels of IL-4, IL-10, and IL-13 in the thymus, but not of IL-1β, INF-γ, TNF-α, and IL-6, suggesting a biological response against cytokine storm.38,39,40,41,42,43,44,45 Thus, we assume that the high efficiency of FNC in treating COVID-19 may be mediated via at least two steps: antiviral action in the thymus and subsequent promotion of immunity against viral infection for the entire body. How the thymus has most of the active forms of FNC is not known. However, this organ and the chemo-to-immune antiviral mode of action can be a rational strategy for designing drugs against SARS-CoV-2.

This drug literally counteracts the exact pathway I have covered for over a year and is a huge part of literally almost every single thing I published in my Substack (PAID hypothesis). In fact, under figure 7 we have an entire paragraph, where the following came from.

As shown in Fig. 7e and Supplementary Fig. 15, the expression of IL-4, IL-13, and IL-10, which were active against IL-6, IL-12, and TNF-α, was elevated in the thymus cells of the FNC -treated viral (+) monkeys (code# 17,368) than those of the untreated ones The expression of RORγt related to Th17 cells was also increased by FNC

Immune staining verified that more IL-4, IL-13, IL-10, and RORγt (Fig. 7e and Supplementary Fig. 15) proteins were expressed in the thymus cells of the FNC-treated monkeys, supporting the results obtained from single-cell sequencing (Fig. 7d).

Of the many pathways that control the differentiation towards Th17, RORγt is one of the “big ones”, so the drug directly acts in the very specific pathway I have been mentioning, researching, and covering for close to a year. One the vaccines induce. “Wait is that it ?”

Obviously not. Read the following piece. And the one about Hematopoietic Stem/Progenitor cells, both of these will be incredibly important later on. In fact, both of those papers are among the most meaningful and important in this whole mess.

SARS-CoV-2, thymic atrophy and impaired T cell development

After reading the post above, you can quite well tell why the Chinese are basically giving a blank approval to the drug, why it is meaningful, why they did Covid 0 (which I oppose btw), and for how long they were aware of this. Without your thymus, and with damaged HSPC you basically have no immune system, so in fact, it is not “AIDS” because with AIDS you have a deficient immune system.

I need to cover other aspects of the KP, and one of its arms IDO for everything else to make sense, and receptors and other aspects of the virus. But now you have a good idea why they used the drug, and how close to target I was (and am with the current things I am covering.

A very big thank you to all supporters here and those who use KoFi =) !