Abstract:Background: Chikungunya is a viral disease that is transmitted by mosquitoes. It is characterized by an acute onset of fever and severe arthralgia. Methods: We describe six cases of acute and post-acute chikungunya in which viral RNA was detected in semen. Conclusions: The most prolonged detection period was 56 days after illness onset. We attempted to cultivate positive semen samples, but virus isolation was unsuccessful in all cases.
“…48,49 Moreover, the virus was found in the urine and semen of patients during infection, which is also suggestive of renal tropism. 50,51 Although the frequency of alterations was much lower for liver markers, they had a higher correlation than all the others, and better spatially organized.…”
Section: Discussionmentioning
confidence: 99%
“…Fittingly, CHIKV is known to replicate in baby hamster kidney cells (BHK‐21 cells) and was found in urine samples, suggesting a possible viral replication in the kidney 48,49 . Moreover, the virus was found in the urine and semen of patients during infection, which is also suggestive of renal tropism 50,51 . Although the frequency of alterations was much lower for liver markers, they had a higher correlation than all the others, and better spatially organized.…”
Chikungunya virus (CHIKV) is an arbovirus (Togaviridae family, Alphavirus genus) that was first identified in 1953 in Tanzania. In 2014, the Asian and East/Central/South/African (ECSA) genotypes were identified in Brazil, although the genotype that spread the most in the following years across the Brazilian territory was the ECSA. The clinical symptoms associated with the infection caused by CHIKV include mainly fever, myalgia, headache, and arthralgia. In infections caused by other arboviruses (such as the ones caused by Dengue and West Nile viruses), changes in biochemical markers are often observed. This study aims to evaluate the biochemical markers profile of kidney and liver injury in acute patients infected with CHIKV. Two groups of correlations were found between the variables analyzed, namely, one between liver enzymes (r = 0.91), and another for kidney markers (r = 0.54–0.66). A significant elevation in the percentage of altered creatinine in CHIKV‐infected patients was observed, followed by uric acid and AST. Altogether, in 8 different comparisons, it was possible to observe statistically significant differences between the levels of the markers when compared to the manifestation of symptoms (presence and absence). These noticeable changes in marker measurements could potentially be connected to the range of clinical symptoms seen in the disease.
“…48,49 Moreover, the virus was found in the urine and semen of patients during infection, which is also suggestive of renal tropism. 50,51 Although the frequency of alterations was much lower for liver markers, they had a higher correlation than all the others, and better spatially organized.…”
Section: Discussionmentioning
confidence: 99%
“…Fittingly, CHIKV is known to replicate in baby hamster kidney cells (BHK‐21 cells) and was found in urine samples, suggesting a possible viral replication in the kidney 48,49 . Moreover, the virus was found in the urine and semen of patients during infection, which is also suggestive of renal tropism 50,51 . Although the frequency of alterations was much lower for liver markers, they had a higher correlation than all the others, and better spatially organized.…”
Chikungunya virus (CHIKV) is an arbovirus (Togaviridae family, Alphavirus genus) that was first identified in 1953 in Tanzania. In 2014, the Asian and East/Central/South/African (ECSA) genotypes were identified in Brazil, although the genotype that spread the most in the following years across the Brazilian territory was the ECSA. The clinical symptoms associated with the infection caused by CHIKV include mainly fever, myalgia, headache, and arthralgia. In infections caused by other arboviruses (such as the ones caused by Dengue and West Nile viruses), changes in biochemical markers are often observed. This study aims to evaluate the biochemical markers profile of kidney and liver injury in acute patients infected with CHIKV. Two groups of correlations were found between the variables analyzed, namely, one between liver enzymes (r = 0.91), and another for kidney markers (r = 0.54–0.66). A significant elevation in the percentage of altered creatinine in CHIKV‐infected patients was observed, followed by uric acid and AST. Altogether, in 8 different comparisons, it was possible to observe statistically significant differences between the levels of the markers when compared to the manifestation of symptoms (presence and absence). These noticeable changes in marker measurements could potentially be connected to the range of clinical symptoms seen in the disease.
“…Cultivating SARS-CoV-2 from specimen can prove the existence of live virus, however, application of virus isolation is limited by many factors [7] , [8] , [9] , [10] , [11] . qRT-PCR is the gold standard method widely used in many diagnostic laboratories in China for the etiological detection of SARS-CoV-2 [12] .…”
“…Several animal models of CHIKV infection have been developed [8][15-20] making it possible to characterize the infection and associated histopathological lesions of the spleen, liver, lymph nodes and muscle, and the development of peri-articular oedema in the acute phase of infection. Some models also allow the study of CHIKV chronic infection [18,[21][22][23][24] as it has been suggested to occur in humans [13,14,25]. A study on partially immunodeficient mice [16] identified fibroblasts of the dermis, muscle and joint capsule, muscle satellite cells, epithelial and endothelial cells of many organs such as liver, brain and spleen as CHIKV cellular targets during the acute phase.…”
First isolated in 1953 in Tanzania, the arthritogenic Chikungunya virus (CHIKV) re-emerged globally in 2005, leading to widespread outbreaks. Unlike other arboviruses, CHIKV predominantly induces symptomatic infections (72-96%), marked by fever, myalgia, polyarthralgia, and rash. Although rarely fatal, atypical forms such as encephalopathies can occur. Notably, 75.4% of patients experience persistent arthralgias for up to three years after the acute phase. Understanding CHIKV's pathophysiology in the joints is challenging due to the difficulties to obtain biological samples. The study employs a mouse model infected with a reporter virus expressing a Nano Luciferase to investigate the disease's transition to chronic arthritis. The murine model reveals viral replication in metatarsi joints, particularly in chondrocytes, confirmed in primary human chondrocytes undergoing viral-induced apoptosis. Ex vivo analysis confirmed viral replication in leg bones and articular cartilages, with histological evidence of focal erosive lesions and periarticular inflammation. The study further utilizes an in vivo imaging mouse model to monitor viral replication over time. Human chondrocytes prove susceptible to CHIKV infection, exhibiting active viral replication, bioluminescence activity, and increased viral production. CHIKV induced apoptosis, the upregulation of markers associated with cartilage remodeling and altered the cytokine production. This comprehensive study, utilizing advanced techniques and models, provides insights into CHIKV's ability to infect articular cartilages, shedding light on the mechanisms of chronic arthritis following infection.
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