Epidemiología molecular del virus Chikungunya en México.

El virus Chikungunya se transmite por la picadura de mosquitos Aedes aegypti y Aedes albopictus [1]. Provoca fiebre alta, dolor en las articulaciones, dolor de cabeza y muscular. Aunque rara vez provoca la muerte, el dolor en las articulaciones puede durar meses o años y en ocasiones convertirse en un dolor crónico y causa de discapacidad para algunas personas. No existe un tratamiento específico ni una vacuna disponible para prevenir la infección de este virus

The zika virus disease: An overview

The zika virus, another re-emerging Flavivirus transmitted to humans by mosquitoes, is responsible for the most recent fever outbreak in the Americas and the Pacific, starting in 2015. The immunologically naïve population in the Americas favors the spread of epidemics. The zika fever is characterized by febrile illness, malaise, conjunctivitis and a maculopapular rash. Similar to other arboviroses recently spread in the Americas, there is no specific or effective antiviral therapy and vaccines are still in trials. The only effective preventive measures consist of individual protection against mosquito bites and vector control. This febrile illness increases the epidemiological and public health challenge existing in America, where the population is already fighting against dengue and chikungunya fever. Disease prevention is important due to the economic burden it entails. The fact of sexual and transfusion virus transmission is a great challenge to overcome. Doctors need to distinguish between dengue, chikungunya and other diseases to give a successful treatment and prevent the disease spreading

Chikungunya virus: A general overview

Chikungunya virus (CHIKV) is a re-emerging mosquito borne alphavirus responsible for the recent outbreak in the Americas. Immunologically naïve population in the Americas favors the spread of epidemics. Chikungunya fever is characterized by an abrupt febrile illness, polyarthralgia and maculopapular rash. In chikungunya fever, shock or severe hemorrhage is very rarely observed; the onset is more acute and the duration of fever is shorter than dengue disease. The pain is much more pronounced and localized to the joints and tendons in chikungunya fever, in comparison to dengue fever. There is no specific and effective antiviral therapy and vaccines are still in trails. The only effective preventive measures consist of individual protection against mosquito bites and vector control. Disease prevention is important due to the economic burden it entails. Clinicians need to distinguish chikungunya fever between dengue fever and other diseases to give a successful treatment and prevent disease spreading

Ebola virus disease 2014

Ebola virus disease was irst described in 1976 originating from the Ebola River in the Democratic Republic of Congo. Since then, Ebola virus has become an important public health threat in Africa, and now it is of great concern worldwide due to the recent outbreaks (9216 cases with 4555 deaths up to October 20th, 2014), and it is so far the largest and deadliest recorded in history. Five Ebola virus species have been identiied (including Zaire, Sudan, Ivory Coast, Reston, and Bundibugyo Ebola virus), and four of them have proved to be highly pathogenic for both human and non-human primates, causing viral hemorrhagic fever with case fatality rates of up to 90%, for which no approved therapeutics or vaccines are currently available. Ebola virus infections are characterized by immune suppression and a systemic inlammatory response that causes impairment of the vascular, coagulation, and immune systems, leading to multiorgan failure and shock, and thus, in some ways, resembling septic shock. The major affected countries, Sierra Leone, Guinea, Liberia, and Nigeria, have been struggling to contain and to mitigate the outbreak. Gene sequencing of the 2014 virus (2014WA) outbreak has demonstrated 98% homology with the Zaire Ebola virus, with a 49% case fatality ratio across the affected countries. In this review the characteristics of the viruses, pathogenesis, diagnosis, treatment, and the cases reported in health care workers (HCW) are described, as well as a summary of outbreaks of the virus since its discovery, including these last two outbreaks in Africa

Whole-exome sequencing in three children with sporadic Blau syndrome, one of them co-presenting with recurrent polyserositis

Blau syndrome (BS) is a rare, chronic autoinflammatory disease with onset before age 4 and mainly characterised by granulomatous arthritis, recurrent uveitis, and skin rash. Sporadic (also known as early-onset sarcoidosis) or familial BS is caused by gain-of-function mutations in the NOD2 gene, which encodes for a multi-task protein that plays a crucial role in the innate immune defense. We report on three Mexican patients clinically diagnosed with BS who exhibited a likely pathogenic variant in NOD2 as revealed by whole-exome sequencing (WES) and Sanger sequencing: two variants (c.1000 C > T/p.Arg334Trp and c.1538 T > C/p.Met513Thr) lie in the ATP/Mg2+ binding site, whereas the other (c.3019dupC/p.Leu1007ProfsTer2) introduces a premature stop codon disrupting the last LRR domain (LRR9) formation; all three variants are consistent with gain-of-function changes. Interestingly, all these patients presented concomitant likely pathogenic variants in other inflammatory disease-related genes, i.e. TLR10, PRR12, MEFV and/or SLC22A5. Although the clinical presentation in these patients included the BS diagnostic triad, overall it was rather heterogeneous. It is plausible that this clinical variability depends partly on the patients’ genetic background as suggested by our WES results. After this molecular diagnosis and given the absence of NOD2 mutations (demonstrated in two trios) and related symptoms in the respective parents (confirmed in all trios), patients 1 and 2 were considered to have sporadic BS, while patient 3, a sporadic BS-recurrent polyserositis compound phenotype. Altogether, our observations and findings underscore the overlapping among inflammatory diseases and the importance of determining the underlying genetic cause by high-throughput methods. Likewise, this study further reinforces a pathogenic link between the here found NOD2 variants and BS and envisages potential additive effects from other loci in these, and probably other patients