HIV1 Specific Neutra™ Antibody Products

Human Immunodeficiency Virus Type 1 (HIV1) is the most prevalent type of HIV, causing most HIV infections worldwide. It is an enveloped retrovirus that uses reverse transcription to incorporate into host DNA. The virus is categorized into four groups (M, N, O, and P), with Group M containing the most common subtypes (A to K). HIV1 particles have a lipid envelope, with glycoproteins (gp120 and gp41) enabling cell entry. Transmission primarily occurs through blood, sexual contact, and from mother to child. HIV1 is a leading cause of the global HIV/AIDS epidemic.

Fig. 1 Structure of HIV1 virion.^1,3

Life Cycle of HIV1

HIV1 infection begins when the virus binds to the CD4 receptor and a coreceptor (CXCR4 or CCR5) on the surface of a target immune cell, usually a T-helper cell. The viral envelope glycoprotein gp120 attaches to CD4, causing a conformational change that allows gp41 to mediate fusion with the host cell membrane. Once inside, the viral RNA is converted into DNA by reverse transcriptase. Integrase integrates the viral DNA into the host genome. The host cell subsequently transcribes and translates the viral genome, generating new viral RNA and proteins. These components assemble and bud off from the host cell, facilitated by protease, which processes viral proteins for maturation.

Immune Response to HIV1 Infection

HIV1 infects vital cells in the human immune system and involves both innate and adaptive mechanisms. Initially, dendritic cells and macrophages detect the virus, activating the innate immune response. As HIV1 targets CD4⁺ T-helper cells, the adaptive immune response kicks in, leading to antibody production by B cells and the recognition of infected cells by cytotoxic T lymphocytes (CTLs). However, HIV1 evades immune detection through rapid mutation, impairing the effectiveness of the immune response. Over time, the virus reduces the number of functional CD4⁺ T-cells, leading to immunodeficiency and increased vulnerability to opportunistic infections, characteristic of AIDS.

Fig. 2 Innate immune sensing of HIV1 in CD4⁺ T cells and myeloid cells.^2,3

Signal Regulation in HIV1 Infection

HIV1 infection involves complex interactions between viral and host cell signaling pathways. Upon binding to CD4 and coreceptors, HIV1 activates intracellular signaling pathways, such as NF-kB and MAPK, which enhance viral replication. HIV1 also disrupts host immune signaling by downregulating key molecules like MHC-I and CD4, preventing effective immune responses. Additionally, the virus exploits cellular pathways to facilitate its replication and survival, such as the activation of NFAT and AP-1 transcription factors. HIV1 proteins, such as Tat and Nef, modulate these pathways, creating a cellular environment conducive to viral persistence and spread.

Anti-HIV1 Neutralizing Antibodies

Antibodies targeting HIV1 aim to neutralize the virus and inhibit its ability to cause infection. Broadly neutralizing antibodies (bnAbs) are a key focus, as they target conserved regions on the HIV1 envelope glycoproteins, particularly the gp120 and gp41 regions. bnAbs, can block the virus from binding to CD4 receptors or prevent viral fusion with host cells. These antibodies work by binding to epitopes that are less prone to mutation, making them effective across different HIV strains. The bnAbs targeting the CD4-binding site of gp120 have been shown to stop up to 90% of HIV1 strains comprising all major viral subtypes. Neutralizing antibodies targeting HIV1 Env have been shown to protect from systemic infection as well as to have an additional antiviral activity that blocks the release of HIV1 by tethering viral particles on the surface of infected cells.

Fig. 3 Targets of anti-HIV1 on the envelope spike protein (Env).⁴

Creative Biolabs provides high-quality anti-HIV1 neutralizing antibody products that are specifically designed for use in a wide range of research applications, including HIV1 detection, neutralization studies, immunoassays, and therapeutic research, ensuring reliable and accurate results.

REFERENCES

1. Dzinamarira, Tafadzwa, et al. "Highlights on the development, related patents, and prospects of lenacapavir: The first-in-class HIV-1 capsid inhibitor for the treatment of multi-drug-resistant HIV-1 infection." Medicina 59.6 (2023): 1041.
2. Yin, Xin, et al. "Sensor sensibility—HIV-1 and the innate immune response." Cells 9.1 (2020): 254.
3. Distributed under Open Access license CC BY 4.0, without modification.
4. Thavarajah, Jannifer Jasmin, Bo Langhoff Hønge, and Christian Morberg Wejse. "The use of broadly neutralizing antibodies (bnAbs) in HIV-1 treatment and prevention." Viruses 16.6 (2024): 911. Distributed under Open Access license CC BY 4.0. The image was modified by extracting and using only part of the original image.