Rosa Rubicondior: The Malevolent Designer - How Creationism Divine Malevolence Brilliantly Designed HIV to Kill Us With

HZI | Decoding HIV's tactics

This should thrill devotees of creationism's intelligent designer because it exposes what a brilliant job it did in designing the human immunosuppressive virus (HIV) that causes the acquired immune deficiency syndrome (AIDS). It was discovered by a group of researchers at the Helmholtz Institute for RNA-based Infection Research (HIRI) in Würzburg and the University of Regensburg, Germany.

They have discovered how HIV hijacks the internal machinery in our cells to ensure its own survival.

Tell me all about the virus HIV, how it evolved and how it infects its victims, please. HIV Overview

Human Immunodeficiency Virus (HIV) is a retrovirus that causes acquired immunodeficiency syndrome (AIDS), a condition in which the immune system becomes severely compromised, leaving individuals vulnerable to opportunistic infections and certain cancers. HIV primarily targets the immune system, particularly CD4+ T cells, which are crucial for immune defense.
Evolution of HIV

Origins:
HIV evolved from Simian Immunodeficiency Viruses (SIVs), which infect non-human primates. Cross-species transmission occurred when humans were exposed to SIV through activities like hunting and handling bushmeat.

HIV-1: Likely originated from SIV in chimpanzees (Pan troglodytes troglodytes) in Central Africa.
HIV-2: Originated from SIV in sooty mangabeys (Cercocebus atys) in West Africa.

Zoonotic Spillover:
The most significant crossover events occurred in the early 20th century. Molecular studies suggest that HIV-1 Group M (responsible for the global pandemic) began spreading among humans in the early 1900s in the Congo basin.
Adaptation to Humans:
After entering humans, HIV underwent mutations that allowed it to infect human cells efficiently and evade immune responses. Its high mutation rate, due to error-prone reverse transcription, facilitates rapid evolution.

How HIV Infects Victims

Entry into the Body:
HIV is transmitted through contact with infected bodily fluids, such as blood, semen, vaginal fluids, rectal fluids, or breast milk. Common routes include unprotected sexual contact, needle sharing, transfusions with contaminated blood, and from mother to child during birth or breastfeeding.
Targeting CD4+ T Cells:
HIV specifically targets immune cells with CD4 receptors, primarily CD4+ T cells, macrophages, and dendritic cells.
Infection Process:

Attachment: HIV binds to CD4 receptors on the host cell via its gp120 envelope protein. Co-receptors (CCR5 or CXCR4) are also required for entry.
Fusion: The virus fuses with the host cell membrane, releasing its RNA and enzymes into the cytoplasm.
Reverse Transcription: HIV’s reverse transcriptase enzyme converts viral RNA into DNA, a process prone to errors that drive genetic variability.
Integration: The viral DNA is integrated into the host genome by the integrase enzyme, establishing a lifelong infection.
Replication: The host cell machinery produces viral proteins and RNA, assembling new virus particles.
Budding: Newly formed viruses bud off from the host cell, often destroying it, and go on to infect other cells.

Immune System Damage:

Over time, HIV depletes CD4+ T cells, weakening the immune system.
This leads to immune exhaustion and susceptibility to opportunistic infections, such as tuberculosis, pneumonia, and fungal infections.

Types and Subtypes

HIV-1:

More virulent and widespread.
Divided into groups (M, N, O, and P), with Group M causing the global pandemic.
Group M is further divided into subtypes (A, B, C, D, etc.). Subtype C is most prevalent worldwide.

HIV-2:

Less transmissible and confined mostly to West Africa.
Progresses more slowly than HIV-1.

Treatment and Prevention

Antiretroviral Therapy (ART):

ART involves a combination of drugs that target different stages of the HIV lifecycle, including reverse transcription, integration, and viral assembly.
While not a cure, ART can suppress viral load to undetectable levels, preventing disease progression and reducing transmission risk.

Prevention:

Condom use and safe sex practices.
Pre-Exposure Prophylaxis (PrEP) and Post-Exposure Prophylaxis (PEP) for high-risk individuals.
Routine HIV testing and early initiation of ART.
Needle exchange programs and safe injection practices.
Prevention of mother-to-child transmission through ART during pregnancy and breastfeeding.

HIV's ability to evolve rapidly and evade immune responses makes it a challenging pathogen to combat, but advances in treatment and prevention have significantly improved outcomes for those living with the virus.

How they discovered this is the subject of an open access paper in the journal Nature Structural & Molecular Biology and a news item from the Helmholtz Centre for Infection Research:

HIRI researchers provide new insights into gene regulation of the virus that causes AIDS
A team of scientists at the Helmholtz Institute for RNA-based Infection Research (HIRI) in Würzburg and the University of Regensburg has unveiled insights into how HIV-1, the virus responsible for AIDS, skillfully hijacks cellular machinery for its own survival. By dissecting the molecular interplay between the virus and its host, the researchers identified novel strategies that HIV-1 employs to ensure its replication while suppressing the host’s cellular defenses. The study was published in the journal Nature Structural and Molecular Biology.
HIV-1, like other viruses, lacks the machinery to produce its own proteins and must rely on the host cell to translate its genetic instructions. After entering host cells, it seizes control of the translation process, which converts messenger ribonucleic acid (mRNA) into proteins.

In this study, we combined ribosome profiling, RNA sequencing and RNA structural probing to map the viral and host translational landscape and pausing during replication of the virus in unprecedented detail.

Neva Caliskan, corresponding author
Helmholtz Institute for RNA-based Infection Research
Helmholtz Centre for Infection Research (HIRI-HZI)
Würzburg, Germany.
[Neva Caliska] is a former group leader at the Helmholtz Institute for RNA-based Infection Research (HIRI) in Würzburg, a site of the Braunschweig Helmholtz Centre for Infection Research (HZI) in cooperation with the Julius-Maximilians-Universität Würzburg (JMU), and is currently the Director of the Department of Biochemistry III at the University of Regensburg.

Cheat Codes of Viral Translation

One of the key findings was the discovery of previously unrecognized elements in HIV-1 RNA called upstream open reading frames (uORFs) and internal open reading frames (iORFs). These “hidden gene fragments” may play a crucial role in fine-tuning the production of viral proteins as well as the interaction with the host immune system.

For instance, uORFs and iORFs can act as regulators, ensuring precise timing and levels of protein synthesis.

Dr. Anuja Kibe, first author
Helmholtz Institute for RNA-based Infection Research
Helmholtz Centre for Infection Research (HIRI-HZI)
Würzburg, Germany.

Another important discovery was an intricate RNA structure near the critical “frameshift site” in the viral genome. This frameshift site is essential for the virus to produce the correct proportions of two key proteins, Gag and Gag-Pol, which are necessary for assembling infectious particles and replication of HIV-1. The researchers demonstrated that this extended RNA fold not only promotes ribosome collisions upstream of the site—a mechanism that appears to regulate translation—but also maintains the frameshifting efficiency. “Our team also showed that targeting this RNA structure with antisense molecules could significantly reduce frameshift efficiency by nearly 40 percent, offering a promising new avenue for antiviral drug development”, reports Caliskan.

A Game of Priorities

Interestingly, our analysis revealed that, while HIV-1 mRNAs are translated efficiently throughout infection, the virus suppresses the protein production of the host, particularly at the translation initiation stage.

Redmond Smyth, co-author Helmholtz Institute for RNA-based Infection Research
Helmholtz Centre for Infection Research (HIRI-HZI)
Würzburg, Germany
Now at Institute of Molecular and Cellular Biology (CNRS)
University of Strasbourg
Strasbourg, France.
This allows HIV-1 to prioritize its own needs while effectively stalling the host defense mechanisms. Thus, the virus can manipulate the host cell machinery in ways that remain robust even under stress conditions.

More Than Traffic Jams

The researchers also observed that ribosomes collide at specific regions of the viral RNA, particularly upstream of the frameshift site.

These collisions are not accidental but are instead tightly regulated pauses that may influence how ribosomes interact with downstream RNA structures.

Florian Erhard, co-author
Faculty of Informatics and Data Science
University of Regensburg
Regensburg, Germany.

Overall, the study provides not only a detailed map of the translational landscape of HIV-1 infected cells but also a wealth of potential targets for therapeutic intervention. The identification of RNA structures and genetic elements critical for viral replication highlights new opportunities for the development of drugs aimed at disrupting these processes.

By understanding how the virus cleverly manipulates our cells, these discoveries will bring us closer to innovative treatments that could one day turn tables and outsmart the virus itself.

Neva Caliskan.

Original publication
Kibe A, Buck S, Gribling-Burrer AS, Gilmer O, Bohn P, Koch T, Mireisz CN, Schlosser A, Erhard F, Smyth RP, Caliskan N. The translational landscape of HIV-1 infected cells reveals key gene regulatory principles. Nature Structural & Molecular Biology (2025), DOI: 10.1038/s41594-024-01468-3

Abstract
Human immunodeficiency virus-1 (HIV-1) uses a number of strategies to modulate viral and host gene expression during its life cycle. To characterize the transcriptional and translational landscape of HIV-1 infected cells, we used a combination of ribosome profiling, disome sequencing and RNA sequencing. We show that HIV-1 messenger RNAs are efficiently translated at all stages of infection, despite evidence for a substantial decrease in the translational efficiency of host genes that are implicated in host cell translation. Our data identify upstream open reading frames in the HIV-1 5′-untranslated region as well as internal open reading frames in the Vif and Pol coding domains. We also observed ribosomal collisions in Gag-Pol upstream of the ribosome frameshift site that we attributed to an RNA structural fold using RNA structural probing and functional analysis. Antisense oligonucleotides designed to alter the base of this structure decreased frameshift efficiency. Overall, our data highlight the complexity of HIV-1 gene regulation and provide a key resource for decoding of host–pathogen interactions upon HIV-1 infection. Furthermore, we provide evidence for a RNA structural fold including the frameshift site that could serve as a target for antiviral therapy.

Kibe, Anuja; Buck, Stefan; Gribling-Burrer, Anne-Sophie; Gilmer, Orian; Bohn, Patrick; Koch, Tatyana; Mireisz, Chiara Noemi-Marie; Schlosser, Andreas; Erhard, Florian; Smyth, Redmond P.; Caliskan, Neva
The translational landscape of HIV-1 infected cells reveals key gene regulatory principles
Nature Structural & Molecular Biology (2025); 10.1038/s41594-024-01468-3.

Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Creationists are in something of a bind here. Most of them will be the same fundamentalists who greeting AIDS as the god's punishment of homosexuals for their 'sinful ways'; they will also be the same creationists who declare that their god wouldn't create organisms that increase the suffering in the world, so it must be due to 'devolution' [sic] caused by 'genetic entropy' made possible by Adam's & Eve's original sin.

But then William A Dembski, high priest of 'specified complexity', makes a case for any complex genetic information that produces functionality being 'specified', and, by inference, the intelligence who specified it, is ID Creationism's intelligent designer.

ID Creationists need to come clean on this. Is the genetic information in viruses and other pathogens 'specified complexity' so evidence of Intelligent design, or is 'specified complexity' evidence of genetic entropy and devolution?

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