TLR3-Activated Monocyte-Derived Dendritic Cells Trigger Progression from Acute Viral Infection to Chronic Disease in the Lung

2021 ◽  
pp. ji2000965
Author(s):  
Xinyu Wang ◽  
Kangyun Wu ◽  
Shamus P. Keeler ◽  
Dailing Mao ◽  
Eugene V. Agapov ◽  
...  
2019 ◽  
Vol 24 (2) ◽  
pp. 161-166 ◽  
Author(s):  
О. A. Uspenskaya ◽  
S. A. Spiridonova

Relevance. One of the causes of chronic disease is herpetic infection, lifelong persistence in the human body and activates the macrophage protection system, which leads to disruption of iron utilization by the cells of the hematopoietic system and the development of anemia of chronic disease. To prove the influence of herpesvirus infection on the occurrence of anemia of chronic disease.Materials and methods. The study involved 75 people suffering from herpes-viral infection. 3 groups were allocated: the frst group (25 people) received acyclovir 1 tablet (200 mg) 5 times a day, 5 days; The 2-nd group (25 people) used famvir for 1 tablet (250 mg) 2 times a day, 5 days; The third group (25 people) – famvir 1 tablet (250 mg) 2 times a day, 5 days and kagocel 2 tablets (12 mg) 3 times a day, 5 days.Result. All subjects examined at the time of treatment showed an increase in the content of IL 1β mRNK and TNF-α and a decrease in mRNK of IL 8 and IL 10; on day 14 of the study, a decrease in IL 1β mRNK and TNF-α mRNK and an increase in IL 10 mRNK. In the study of erythrocyte indices – the average volume of erythrocytes and the average hemoglobin content in erythrocyte and the parameters of iron-serum iron metabolism and the total iron binding capacity of the serum, slight deviations from the norm were obtained.Conclusions. Thus, we concluded that the cause of anemia, in addition to the lack of iron, can be chronic herpesvirus infection, and thus timely treatment of a viral infection excludes the use of ferrotherapy.


immuneACCESS ◽  
2018 ◽  
Author(s):  
WS DeWitt ◽  
RO Emerson ◽  
P Lindau ◽  
M Vignali ◽  
TM Snyder ◽  
...  

2012 ◽  
Vol 2 (1) ◽  
pp. 50-52
Author(s):  
Rohit B Gadda ◽  
Neha Patil ◽  
Rohini Salvi

Abstract Herpes zoster is a common acute viral infection caused by reactivation of Varicella-Zoster virus. Acute pain of herpes zoster lowers the quality of life and interferes with day to day activities. We report a case of herpes zoster in a 68 year old, healthy male patient in which the prodromal symptoms started as toothache. This case highlights the importance of a thorough dental history and examination in patients with toothache.


2019 ◽  
Vol 20 (11) ◽  
pp. 2811 ◽  
Author(s):  
Marta Corsetti ◽  
Gabriella Ruocco ◽  
Serena Ruggieri ◽  
Claudio Gasperini ◽  
Luca Battistini ◽  
...  

Background: Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system. The cause of multiple sclerosis is unknown but there are several evidences that associate the genetic basis of the disease with environmental causes. An important association between viral infection and development of MS is clearly demonstrated. Viruses have a strong impact on innate immune cells. In particular, myeloid dendritic cells (mDCs) and plasmacytoid dendritic cells (pDCs), are able to respond to viruses and to activate the adaptive immune response. Methods: In this study we mimic viral infection using synthetic single-strand RNA, Resiquimod, and we compared the response of both DC subsets derived from healthy donors and MS patients by characterizing the expression of costimulatory molecules on the DC surface. Results: We found that pDCs from MS patients express higher levels of OX40-L, HLA-DR, and CD86 than healthy donors. Moreover, we found that blood cells from MS patients and healthy donors upon Resiquimod-stimulation are enriched in a subpopulation of pDCs, characterized by a high amount of costimulatory molecules. Conclusion: Overall, these results indicate that activation of pDCs is enhanced in MS, likely due to a latent viral infection, and that costimulatory molecules expressed on pDCs could mediate a protective response against the viral trigger of autoimmunity.


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