F Rosa Rubicondior: Malevolent Designer News - How HIV Research is Trying to Overcome the "Designer's" Devilish Malevolence

Monday 6 November 2023

Malevolent Designer News - How HIV Research is Trying to Overcome the "Designer's" Devilish Malevolence

Human Immunodeficiency Virus (HIV)

Pinpointing HIV immune response

The traditional creationist double-think response, when presented with evidence of malevolent design in the form of parasites such as pathological viruses, bacteria, protozoa or worms, etc., is to blame something called 'Sin' for their creation, absolving their proclaimed intelligent [sic] designer of any culpability, while maintaining that everything living must be attributed to their god because it is the only entity capable of designing living organisms.

However, in the case of HIV, the virus that causes Acquired Immune Deficiency Syndrome (AIDS) in humans, they greeted it with barely concealed jubilation in their caring Christian way, declaring it to be a 'Gay Plague' sent by their god to punish homosexuals, so they now can't blame Satan or 'Sin' for its creation. A case of being hoist by their own petard.

And to add to creationists' embarrassment, they also believe the human immune system that HIV evades then suppresses, was designed by their, allegedly perfect, omniscient designer to protect us from the parasites it created to harm or kill us, in which case, HIV, like so many other pathogens, is a testament to its incompetence.

HIV is one of a group of RNA retroviruses that can hide from our immune system by inserting a DNA version of their RNA into our DNA using the enzyme reverse transcriptase that they bring with them. Once inserted, the virus looks for all the world like just another chunk of junk DNA. Indeed, like most species, our DNA contains lots of mutated and harmless relics of these retrovirus from our evolutionary history.

Now though, medical science, in trying to do what seems beyond the capability of creationism's putative omnipotent intelligent [sic] designer is closing in on just how HIV manages to evade and suppress our immune system, and how our immune system responds to it.

In a paper just published open access in the journal Science Communications a team of scientists led by Ruy M. Ribeiro, a theoretical biologist at Los Alamos National Laboratory, Los Alamos, NM, USA has shown, using experiments on Macaque monkeys and mathematical modelling, that, although the body's immune system does succeed in suppressing virus production and in killing infected cells, the response only last for a very short time at the start of infection.

The Macaques used in the experiment were infected with a close relative of HIV known as Simian Immunodeficiency Virus (SIV). Macaques' immune systems respond to SIV the same way that human immune systems respond to HIV.

The key to controlling infection and eventually curing it, is in understanding how the body responds in the early stages of infection and, more importantly, why it gives up. Enhancing that process and maintaining it for longer may result in elimination of the virus altogether.

The immune system can’t eliminate an HIV infection, but pinpointing the existing mechanism by which it is to some extent controlling HIV is very important for designing treatments to enhance that mechanism. If we can modulate the immune system to help control HIV better, we may be able to cure the disease at some point.

Ruy M. Ribeiro, Corresponding author
Theoretical Biology and Biophysics Group
Los Alamos National Laboratory, Los Alamos, NM, USA.
By focusing on the immune response mediated by cells in the immune system known as CD8+ T cells, the team have also resolved a question about their role in an immune response: do they just kill infected cells or do they stimulate infected cells to fight the virus without killing the cells. The answer turns out to be "a little of both".

The state of knowledge of the function of CD8+ T cells (also called killer T cells) in 2021 is related by ChatGPT 3.5:
In the human immune system, what are CD8+ T cells and what is their role? CD8+ T cells, also known as cytotoxic T cells or killer T cells, are a type of white blood cell that plays a critical role in the human immune system. They are a subset of T lymphocytes, a type of immune cell, and are an essential part of the adaptive immune response. CD8+ T cells primarily function to eliminate infected or abnormal cells in the body. The main role of CD8+ T cells is to recognize and destroy cells that have been infected by viruses or other intracellular pathogens. They do this through a process called cell-mediated immunity. Here's how it works:
  1. Antigen recognition: CD8+ T cells are activated when they encounter antigens, which are small fragments of proteins from pathogens presented on the surface of infected cells. These antigens are typically presented by specialized antigen-presenting cells, such as dendritic cells.
  2. Activation: When a CD8+ T cell recognizes an antigen that matches its specific receptor (T cell receptor), it becomes activated. This activation leads to the proliferation of CD8+ T cells, generating a population of effector T cells that can target the infected cells.
  3. Target cell destruction: Activated CD8+ T cells are highly cytotoxic. They release cytotoxic proteins, such as perforin and granzymes, which can enter the infected cell and trigger its apoptosis (programmed cell death). This process effectively kills the infected cell and prevents the pathogen from replicating within it.
  4. Memory: After the infection is cleared, some of the CD8+ T cells become memory T cells. These memory cells remain in the body and can provide a faster and more effective immune response if the same pathogen infects the body again in the future. This is the basis for immunological memory.
CD8+ T cells are an essential component of the adaptive immune system, working in coordination with other immune cells like CD4+ T cells, B cells, and antibodies to protect the body from a wide range of infections and diseases. Their ability to target and eliminate infected cells is critical for the body's defense against intracellular pathogens, such as viruses.
In the experiments on infected Macaques, they were divided into three groups: one group received a drug that blocked the virus from entering into the host cell's DNA; another group were given an antibody that eliminates the CD8+ T cells and the third group received both. The Macaques' viral load was then measured and the results fed into a mathematical model to determine the effects of the different immune responses. From the model the researchers inferred the most relevant immune mechanisms that more closely described the observed data.

The results are published in Nature Communications. Part of the Introduction is reprinted to illustrate the complexity of the problem.:

Whether CD8+ T lymphocytes control human immunodeficiency virus infection by cytopathic or non-cytopathic mechanisms is not fully understood. Multiple studies highlighted non-cytopathic effects, but one hypothesis is that cytopathic effects of CD8+ T cells occur before viral production. Here, to examine the role of CD8+ T cells prior to virus production, we treated SIVmac251-infected macaques with an integrase inhibitor combined with a CD8-depleting antibody, or with either reagent alone. We analyzed the ensuing viral dynamics using a mathematical model that included infected cells pre- and post- viral DNA integration to compare different immune effector mechanisms. Macaques receiving the integrase inhibitor alone experienced greater viral load decays, reaching lower nadirs on treatment, than those treated also with the CD8-depleting antibody. Models including CD8+ cell-mediated reduction of viral production (non-cytolytic) were found to best explain the viral profiles across all macaques, in addition an effect in killing infected cells pre-integration (cytolytic) was supported in some of the best models. Our results suggest that CD8+ T cells have both a cytolytic effect on infected cells before viral integration, and a direct, non-cytolytic effect by suppressing viral production.


Understanding the host immune response against HIV/SIV infection is essential for developing effective therapeutic and preventive strategies. Unfortunately, HIV continuously evades and subdues the host’s immune responses, muddling our attempts at elucidating the nature of the immune mechanisms needed to control infection. Examples of HIV evasion strategies include: (i) undergoing rapid mutation of its proteins due to host immune pressures to effectively evade host adaptive responses1,2,3; (ii) inducing down regulation of MHC-I expression through the viral protein Nef to reduce host cytotoxic capabilities to target infected cells4; (iii) taking advantage of virus-specific adaptive responses that generate activated CD4+ T cells, the preferential target of HIV, to propagate the infection5; (iv) chronically stimulating the immune system, thus resulting in production of nonfunctional exhausted cytotoxic T lymphocytes (CTLs)6,7. As such, there is uncertainty regarding which immune response should be emphasized in current research efforts.

Of the various immune responses against HIV, the response exerted by CD8+ T cells has been shown to be critical for control of HIV/SIV8. This is supported by: (i) the temporal association that exists between the increase in virus-specific CD8+ T cell responses and the post-peak decline in plasma viremia9,10; (ii) the CD8+ CTLs ability to suppress new infections in vitro11,12; (iii) the virus escape mutations that consistently arise in response to the host CD8+ T cell response during all stages of infection1,2,13,14; (iv) the strong association between specific host MHC-I alleles and HIV/SIV disease progression15; and (v) the association of circulating escape mutants with the prevalence of specific HLAs in the population16,17. Experimental in vivo CD8+ cell depletion studies in SIV-infected macaques have strengthened this argument and provided more direct evidence for the role of CD8+ cells in HIV infection18,19,20,21,22,23,24,25,26,27,28. CD8+ cell depletion results in a rapid and sustained rebound of plasma viremia, which is controlled when CD8+ cells are restored. These results are consistent in many models of SIV infection: elite controller18,29, nonpathogenic30, rapid progressor21,31, antiretroviral treated20,22,23 and untreated models19,24,26,32. Accordingly, understanding the mechanisms of action of CD8+ cells and identifying strategies to boost CD8+-specific immune responses is a key priority, both for HIV vaccine and cure research.

Although CD8+ cells hold strong potential for cure efforts, their specific mechanism(s) of action is not well understood8. CD8+ CTLs could exert a direct cytotoxic response against viral-infected cells via release of granzyme/perforin and/or stimulation of the Fas/FasL pathway33,34. Alternatively, CD8+ cells could act by interfering with de novo infection or the release of new virions through soluble antiviral factors, including the CCR5-binding proteins MIP-1α, MIP-1β, RANTES, the cellular anti-HIV factor (CAF), α-defensins, and other factors35,36,37. To help shed light on this question, two groups studied the lifespan of SIV-infected cells after nucleotide reverse transcriptase inhibitor (NRTI) treatment, either in the presence or absence of CD8+ cells. They showed that the average lifespan was not different with or without CD8+ cells, concluding that CD8+ CTLs do not exert a cytolytic effect on infected cells20,23. Another study quantified the lifespan of infected cells after antiretroviral treatment in infected people with different HLA background, both favorable and unfavorable for HIV progression38. These studies found no difference in the lifespan of infected cells and concluded that protective CD8+ T cells may exert their effect before onset of productive infection, or via noncytolytic mechanisms, but none of them directly demonstrated this20,23,38. These data have both been corroborated and challenged39,40,41,42,43, leaving the field to question what the true mechanism(s) of action of CD8+ T cells is against HIV. … (read more)

I wonder if a creationist will ever be brave enough to answer the questions arising from HIV and its Devilishly clever 'design':
  1. Was it created by 'Sin' or Satan or was designed by their god to punish humans for 'sin'?
  2. If the latter, why should this evidently pestilential god be regarded as a malevolence, forever designing new ways to increase suffering in the world and reduce happiness as an indiscriminate punishment for 'sins' that it could just forgive us for if it so chose?
  3. If the former, why would Satan or 'Sin' be punishing people for 'sinning'?
  4. Why is it preferable for people to think of creationism's god as a pestilential malevolence, rather than have people accept that viruses like HIV and other parasitic pathogens are the product of a natural, mindless processes in which neither gods nor 'Sin' were involved?

Thank you for sharing!

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