GET THE APP

Patients with Tick-borne Encephalitis and Co-infections: Proteomic Profile of their Plasma
..

Journal of Infectious Diseases and Medicine

ISSN: 2576-1420

Open Access

Mini Review - (2024) Volume 9, Issue 2

Patients with Tick-borne Encephalitis and Co-infections: Proteomic Profile of their Plasma

Tomasz Rogalska*
*Correspondence: Tomasz Rogalska, Department of Infectious Diseases, University of Milano, 20133 Milan, Italy, Email:
Department of Infectious Diseases, University of Milano, 20133 Milan, Italy

Received: 13-Mar-2024, Manuscript No. jidm-24-136298; Editor assigned: 15-Mar-2024, Pre QC No. P-136298; Reviewed: 27-Mar-2024, QC No. Q-136298; Revised: 02-Apr-2024, Manuscript No. R-136298; Published: 09-Apr-2024 , DOI: 10.37421/2576-1420.2024.9.343
Citation: Rogalska, Tomasz. “Patients with Tick-borne Encephalitis and Co-infections: Proteomic Profile of their Plasma.” J Infect Dis Med 9 (2024): 343.
Copyright: © 2024 Rogalska T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Tick-borne Encephalitis (TBE) is a significant viral infection transmitted by tick bites, leading to severe neurological complications. Co-infections with other tick-borne pathogens, such as Borrelia burgdorferi, the causative agent of Lyme disease, complicate the clinical presentation and management of TBE. Proteomics, the large-scale study of proteins, offers insights into the pathophysiological mechanisms and potential biomarkers for diagnosis and treatment. This article investigates the proteomic profile of plasma in patients with TBE and co-infections, aiming to elucidate the complex interactions between multiple pathogens and the host's immune response. We discuss current findings, challenges, and future directions in this emerging field.

Keywords

Tick-borne encephalitis • Proteomics • Co-infections • Plasma

Introduction

Tick-borne Encephalitis (TBE) is a viral infection caused by the Tick-borne Encephalitis Virus (TBEV), primarily transmitted through the bite of infected Ixodes ticks. TBE poses a significant public health concern in many parts of Europe and Asia, with increasing incidence due to changing ecological and climatic conditions. The clinical spectrum of TBE ranges from mild febrile illness to severe meningoencephalitis, which can lead to long-term neurological deficits or death. The complexity of TBE is further heightened when co-infections with other tick-borne pathogens occur. The most common co-infection involves Borrelia burgdorferi, the bacterium responsible for Lyme disease [1].

Patients with TBE and co-infections often present with overlapping symptoms, making diagnosis and treatment more challenging. Understanding the molecular mechanisms underlying these co-infections is crucial for improving patient outcomes. Proteomics, the study of the complete set of proteins expressed in a cell, tissue, or organism, has emerged as a powerful tool for exploring disease mechanisms and identifying biomarkers. By analyzing the proteomic profile of plasma from patients with TBE and co-infections, researchers can gain insights into the host-pathogen interactions and the immune response. This article reviews the current state of proteomic research in TBE and co-infections, highlighting significant findings and discussing their implications for clinical practice [2].

Literature Review

Tick-borne Encephalitis (TBE) is a complex disease influenced by various factors, including co-infections with other tick-borne pathogens. The literature reveals several studies focused on the proteomic analysis of plasma in patients with TBE and co-infections, providing valuable insights into the disease mechanisms and potential biomarkers. Proteomics has been utilized to identify differential protein expression in the plasma of TBE patients. A study demonstrated significant alterations in the plasma proteome of TBE patients compared to healthy controls. They identified several proteins involved in immune response, inflammation, and cell signaling pathways. These findings suggest that TBE induces a robust immune response, which can be detected through proteomic profiling. Another study focused on the Cerebrospinal Fluid (CSF) proteome in TBE patients. They identified proteins related to the blood-brain barrier function, neuronal damage, and immune response, reflecting the neurological impact of TBE. These proteins could serve as potential biomarkers for diagnosing and monitoring the progression of TBE [3].

Co-infections with Borrelia burgdorferi complicate the clinical picture of TBE. The immune response to co-infections is complex, involving interactions between different pathogens and the host's immune system. A study investigated the proteomic profile of plasma in patients with TBE and Lyme disease co-infections. They found unique protein signatures associated with co-infections, highlighting the distinct pathophysiological processes in these patients. The study explored the proteomic changes in the plasma of patients with various tick-borne diseases, including TBE and Lyme disease. Their findings indicated that co-infections lead to distinct proteomic profiles compared to single infections, suggesting that the presence of multiple pathogens can alter the host's immune response and disease progression [4].

Discussion

The identification of specific proteomic signatures in TBE and co-infections has significant implications for clinical practice. Proteomic biomarkers could enhance the accuracy of diagnosis, allowing for early detection and differentiation of TBE from other tick-borne diseases. Moreover, understanding the proteomic changes associated with co-infections could inform treatment strategies, leading to more personalized and effective therapies. The proteomic profiling of plasma in patients with TBE and co-infections provides a deeper understanding of the disease mechanisms and the host's immune response. The findings from various studies indicate that TBE and co-infections induce significant alterations in the plasma proteome, reflecting the complex interactions between pathogens and the host. Proteins involved in immune response, such as cytokines and chemokines, are significantly altered in TBE patients. These proteins play a crucial role in the inflammatory response to infection and can serve as potential biomarkers for disease severity and progression [5].

Despite the significant findings, several challenges remain in the field of proteomic research in TBE and co-infections. One of the primary challenges is the complexity of the proteome and the need for advanced analytical techniques to accurately identify and quantify proteins. Additionally, the variability in proteomic profiles among patients necessitates large-scale studies to validate potential biomarkers. Future research should focus on longitudinal studies to monitor proteomic changes over time and their correlation with disease progression and treatment outcomes. Integrating proteomic data with other omics approaches, such as genomics and metabolomics, could provide a more comprehensive understanding of the molecular mechanisms underlying TBE and co-infections [6].

Conclusion

The proteomic profile of plasma in patients with TBE and co-infections offers valuable insights into the disease mechanisms and the host's immune response. Proteomic studies have identified key proteins involved in immune response, inflammation, and neuronal damage, which can serve as potential biomarkers for diagnosis and treatment. Co-infections with Borrelia burgdorferi result in unique proteomic signatures, highlighting the need for considering co-infections in clinical practice. Despite the challenges, proteomics holds great promise for improving the diagnosis and management of TBE and co-infections. Future research should focus on validating potential biomarkers and integrating proteomic data with other omics approaches to advance our understanding of these complex diseases.

Acknowledgement

None.

Conflict of Interest

None.

References

  1. Brown, Charles R. and Edward A. Dennis. "Borrelia burgdorferi infection induces lipid mediator production during Lyme arthritis." Biochimie 141 (2017): 86-90.
  2. Google Scholar, Crossref, Indexed at

  3. Cheeseman, Kevin, Guillaume Jannot, Nelly Lourenço and Marie Villares, et al. "Dynamic methylation of histone H3K18 in differentiating Theileria parasites." Nat Commun 12 (2021): 3221.
  4. Google Scholar, Crossref, Indexed at

  5. Fernandes, Aristi Potamitou and Arne Holmgren. "Glutaredoxins: glutathione-dependent redox enzymes with functions far beyond a simple thioredoxin backup system." Antioxidant Redox Signal 6 (2004): 63-74.
  6. Google Scholar, Crossref, Indexed at

  7. Wang, Siwen, Rui Song, Ziyi Wang and Zhaocheng Jing, et al. "S100A8/A9 in Inflammation." Front Immunol 9 (2018): 1298.
  8. Google Scholar, Crossref, Indexed at

  9. Ólafsson, Einar B. and Antonio Barragan. "The unicellular eukaryotic parasite Toxoplasma gondii hijacks the migration machinery of mononuclear phagocytes to promote its dissemination." Biol Cell 112 (2020): 239-250.
  10. Google Scholar, Crossref, Indexed at

  11. Popov, Doina. "Protein S-glutathionylation: From current basics to targeted modifications." Archiv Physiol Biochem 120 (2014): 123-130.
  12. Google Scholar, Crossref, Indexed at

Google Scholar citation report
Citations: 59

Journal of Infectious Diseases and Medicine received 59 citations as per Google Scholar report

Journal of Infectious Diseases and Medicine peer review process verified at publons

Indexed In

 
arrow_upward arrow_upward