In addition to the acute symptoms after infection, patients and society are also being challenged by the long-term effects of COVID-19, known as long COVID. Oxidative stress, as a pivotal point in the pathophysiology of COVID-19, could potentially be also involved in the development of the post-COVID syndrome. The aim of the present study was to evaluate the relationship between changes in oxidative status and the persistence of long-COVID symptoms in workers with a previous mild COVID-19 infection. A cross-sectional study was conducted among 127 employees of an Italian university (80 with a previous COVID-19 infection, and 47 healthy subjects). The TBARS assay was used to detect malondialdehyde serum levels (MDA), while total hydroperoxide (TH) production was measured by a d-ROMs kit. A significant difference in mean serum MDA values was found between previously infected subjects and healthy controls and (4.9 µm vs. 2.8 µm, respectively). Receiver–operating characteristic (ROC) curves showed high specificity and good sensibility (78.7% and 67.5%, respectively) for MDA serum levels. A random forest classifier identified the hematocrit value, MDA serum levels, and IgG titer against SARS-CoV-2 as features with the highest predictive value in distinguishing 34 long-COVID from 46 asymptomatic post-COVID subjects. Oxidative damage persists in subjects with previous COVID-19 infection, suggesting a possible role of oxidative stress mediators in the pathogenesis of long COVID.

We assessed the presence ofRickettsiaspp.,Coxiella burnetiiandAnaplasma phagocytophilumin reptiles, their ectoparasites and in questing ticks collected in a nature preserve park in southern Italy, as well as in a peri-urban area in another region. We also investigated the exposure to these pathogens in forestry workers, farmers and livestock breeders living or working in the nature preserve park given the report of anecdotal cases of spotted fever rickettsioses.Rickettsiaspp. were molecularly detected inPodarcis muralisandPodarcis siculuslizards (i.e., 3.1%), inIxodes ricinus(up to 87.5%) and inNeotrombicula autumnalis(up to 8.3%) collected from them as well as inI.ricinuscollected from the environment (up to 28.4%).Rickettsia monacensiswas the most prevalent species followed byRickettsia helvetica. An undescribed member of the family Anaplasmataceae was detected in 2.4% and 0.8% of the reptiles and ectoparasites, respectively. Sera from human subjects (n = 50) were serologically screened and antibodies toRickettsiaspp. (n = 4; 8%),C.burnetti(n = 8; 16%) andA.phagocytophilum(n = 11; 22%) were detected. Two ticks collected from two forestry workers were positive for spotted fever group (SFG) rickettsiae.Ixodes ricinusis involved in the transmission of SFG rickettsiae (R.monacensisandR.helvetica) in southern Europe and lizards could play a role in the sylvatic cycle ofR.monacensis, as amplifying hosts. Meanwhile,N.autumnaliscould be involved in the enzootic cycle of some SFG rickettsiae among these animals. People living or working in the southern Italian nature preserve park investigated are exposed to SFG rickettsiae,C.burnetiiandA.phagocytophilum.

Background: Homocysteine is a sulfur amino acid whose metabolism is activated in two pathways: remethylation to methionine, which requires folate and vitamin B₁₂, and transsulfuration to cystathionine, which needs pyridoxal-5’-phosphate. High homocysteine level increases the risk of developing heart disease, stroke, peripheral vascular diseases, and cognitive impairment. Some evidence showed that exposure to these metals increased plasma homocysteine levels. Methods: A systematic review was carried out to clarify the relationship between homocysteine blood levels and exposure to toxic heavy metals (Lead, Cadmium, Mercury, and Chromium). Results: The results of this systematic review indicate that exposure to Pb, Cr, Cd, and Hg is connected with nonphysiological homocysteine levels or vitamin B₁₂ and folate serum concentrations. Conclusions: These findings reinforce the importance of involvement in exposure to heavy metals in homocysteine metabolism. This supports the role of blood metals as potential upstream modifiable risk factors to prevent the development of other established risk factors as hyperhomocysteinemia.