CMV Specific Neutra™ Antibody Products

Cytomegalovirus (CMV) is a ubiquitous herpesvirus with humans and monkeys acting as its natural hosts. It can lead to a variety of health issues, ranging from mild or no symptoms to severe conditions, particularly in immunocompromised individuals and newborns. Risk factors include weakened immunity and close contact. Symptoms vary, including fever, fatigue, and organ-specific issues. Transmission occurs through bodily fluids. CMV's epidemiology reflects widespread exposure, with seroprevalence increasing with age.

Structure and Genome of CMV

CMV is a sizable, enveloped virus with a double-stranded DNA genome. Its structure includes a capsid, tegument, and envelope. The capsid contains the linear dsDNA genome, approximately 235 kb, one of the largest among herpesviruses. The tegument, situated between the capsid and envelope, contains proteins crucial for viral replication. The envelope embeds glycoproteins essential for cell entry. The genome encodes numerous proteins involved in immune evasion and replication.

Fig. 1 Schematic of CMV structure.Distributed under CC BY-SA 2.5, from Wiki, without modification.

Life Cycle of CMV

Viral replication is nuclear and lysogenic. CMV enters cells via receptor-mediated fusion. Following entry, the capsid releases the DNA into the nucleus. Early genes are transcribed, leading to the synthesis of regulatory proteins. DNA replication occurs, followed by late gene expression, encoding structural proteins. Capsid assembly takes place in the nucleus. The virus exits the nucleus by budding through the inner nuclear membrane, gaining its tegument and envelope. Mature virions are released via exocytosis. CMV can establish latency in various cell types, like monocytes and hematopoietic stem cells.

Pathogenic Mechanism of CMV

CMV pathogenesis involves immune modulation and direct cellular damage. The virus evades immune responses by downregulating MHC class I and II molecules, hindering antigen presentation. CMV also encodes proteins that interfere with cytokine signaling and apoptosis. Direct cellular damage arises from viral replication, causing cytomegaly (enlarged cells) and inflammation. In immunocompromised individuals, uncontrolled viral replication leads to organ damage, including retinitis, pneumonitis, and encephalitis. CMV infections are commonly linked to the salivary glands in humans and other mammals. Congenital CMV infection can cause severe developmental abnormalities due to fetal tissue damage.

Fig. 2 Immune response to CMV infection in the brain.¹

Anti-CMV Neutralizing Antibodies

Neutralizing antibodies targeting CMV are being developed as potential therapies. These antibodies can prevent cell-to-cell spread and reduce viral load. Some neutralizing antibodies have shown the ability to neutralize HCMV infection and protect against congenital CMV infection. Researchers have identified several viral antigens that are targets for neutralizing antibodies, including proteins like gH, gB, and UL128-131 complex. Besides, antibodies targeting CMV have been developed for detection applications, like ELISA and WB assays. ELISA detects anti-CMV IgG and IgM, indicating past or recent infection. WB confirms ELISA results by identifying specific viral proteins, providing a more detailed serological profile. Research shows that these antibody-based assays are essential for diagnosing CMV infection and monitoring immune status.

Fig. 3 Workflow of a broadly anti-CMV neutralizing antibodies development.²

With our skilled team of experts and cutting-edge antibody platform, Creative Biolabs provides a diverse selection of high-quality anti-CMV neutralizing antibodies tailored to meet your specific research requirements.

REFERENCES

1. Krstanović, Fran, et al. "Cytomegalovirus infection and inflammation in developing brain." Viruses 13.6 (2021): 1078. Distributed under Open Access license CC BY 4.0, without modification.
2. Parsons, Andrea J., et al. "Development of broadly neutralizing antibodies targeting the cytomegalovirus subdominant antigen gH." Communications Biology 5.1 (2022): 387. Distributed under Open Access license CC BY 4.0. The image was modified by extracting and using only part of the original image.