Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections are widely distributed throughout the world. EBV is linked to various hematological and autoimmune disorders whereas CMV might play important role in the progression of chronic hematological diseases, such as hemoglobinopathies, lymphomas, myelomas, hemophilia, and aplastic and sickle cell anemia. Both viruses produce a viral homolog of human interleukin-10 that can cause general suppression of immune response, increasing susceptibility to other infections. These viruses can remain latent in the host cells and be reactivated when the host immune system is compromised. Studies showing the impact of CMV and EBV infections on hematological disorders are scarce and unclear in the context of coinfection. This review intends to present the biology, prevalence, and impact of CMV and EBV infections in patients with hematological diseases.

Background The Duffy glycoprotein acts as the entry point for merozoites of Plasmodium vivax in the invasion of red blood cells. The host–parasite relationship has revealed new perspectives regarding the association between Duffy polymorphisms that can impact both the parasite density of this Plasmodium and the symptoms of this type of malaria. This study investigates the impact of Duffy polymorphisms on parasite density in patients infected with P. vivax in the Brazilian Amazon region. Methods Genotypes and Duffy polymorphism allele frequencies were compared in 287 patients with malaria, presenting low, medium and high density of P. vivax . The diagnosis of malaria was performed using a specialized team with a standardized clinical-laboratory method, while the Duffy genotyping was performed through the Bead Chip BioArray system. Both teams are reference services in Brazil. Results The FY*01 and FY*02 alleles were found in all three parasite density classes: low, medium and high, but when these alleles form genotypes with FY*02N.01 and FY*02W.01 alleles, they are found only in patients with low parasite density and low symptomatology. Another interesting finding found in this study is the presence of the genotype FY*02N.01 / FY*02W.01 in one of the patients, presenting a very low parasite density and malaria considered subclinical, a genotype which had not been previously described in the literature. Conclusion The presence of FY*02N.01 and FY*02W.01 alleles may have an impact on the reduction of clinical manifestations in malaria, leading to the development of subclinical malaria, making the infected individual an undetected natural reservoir, which may hinder the eradication of malaria in the Amazon.

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Chryseobacterium indologenes is an emerging nosocomial pathogen that produces IND-type chromosomal metallo-beta-lactamase. The phenotype and molecular aspects of two multidrug resistant C. indologenes strains and the analysis of the tertiary structure of the IND enzyme were studied. Identification of species and susceptibility tests were performed using the Vitek-2 compact. Chromosomal and plasmid DNA were extracted using PureLinkÔ Genomic DNA Mini Kit and PureLink Quick Plasmid Miniprep Kit, and the sequencing was performed using ABI 3130 genetic analyzer. Two strains were isolated and are registered as P-23 and P-113. Of the two, P-113 was sensitive to ciprofloxacin and cefepime only, whereas the P-23 showed reduced sensitivity to ceftazidime, ciprofloxacin, and tigecycline. The genetic analysis of both isolates identified the presence of the bla IND-like gene, with similarity to IND-3 and IND-8 alleles. The IND-3 identified in the P-133 sample presented a single mutation at position T355G, which corresponds to a nonsynonymous substitution of the amino acid at position 119 (Ser/Ala). The phylogenetic analysis of INDs showed lineages that are circulating in Asian and European countries. These results emphasize the need for effective preventive actions to avoid the dissemination of this type of pathogen in the hospital environment.

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