Andes hantavirus (ANDV) causes hantavirus cardiopulmonary syndrome in Chile and is the only hantavirus for which person-to-person transmission has been proven. We describe an outbreak of 5 human cases of ANDV infection in which symptoms developed in 2 household contacts and 2 health care workers after exposure to the index case-patient. Results of an epidemiologic investigation and sequence analysis of the virus isolates support person-to-person transmission of ANDV for the 4 secondary case-patients, including nosocomial transmission for the 2 health care workers. Health care personnel who have direct contact with ANDV case-patients or their body fluids should take precautions to prevent transmission of the virus. In addition, because the incubation period of ANDV after environmental exposure is longer than that for person-to-person exposure, all persons exposed to a confirmed ANDV case-patient or with possible environmental exposure to the virus should be monitored for 42 days for clinical symptoms.

Andes virus (ANDV) is the only hantavirus transmitted between humans through close contact. We detected the genome and proteins of ANDV in breast milk cells from an infected mother in Chile who transmitted the virus to her child, suggesting gastrointestinal infection through breast milk as a route of ANDV person-to-person transmission.

Background: Andes virus (ANDV), a rodent-borne Hantavirus, is the major etiological agent of Hantavirus cardiopulmonary syndrome (HCPS) in South America, which is mainly characterized by a vascular leakage with high rate of fatal outcomes for infected patients. Currently, neither specific therapy nor vaccines are available against this pathogen. ANDV infects both dendritic and epithelial cells, but in despite that the severity of the disease directly correlates with the viral RNA load, considerable evidence suggests that immune mechanisms rather than direct viral cytopathology are responsible for plasma leakage in HCPS. Here, we assessed the possible effect of soluble factors, induced in viral-activated DCs, on endothelial permeability. Activated immune cells, including DC, secrete gelatinolytic matrix metalloproteases (gMMP-2 and -9) that modulate the vascular permeability for their trafficking.Methods: A clinical ANDES isolate was used to infect DC derived from primary PBMC. Maturation and pro-inflammatory phenotypes of ANDES-infected DC were assessed by studying the expression of receptors, cytokines and active gMMP-9, as well as some of their functional status. The ANDES-infected DC supernatants were assessed for their capacity to enhance a monolayer endothelial permeability using primary human vascular endothelial cells (HUVEC).Results: Here, we show thatin vitroprimary DCs infected by a clinical isolate of ANDV shed virus RNA and proteins, suggesting a competent viral replication in these cells. Moreover, this infection induces an enhanced expression of soluble pro-inflammatory factors, including TNF-α and the active gMMP-9, as well as a decreased expression of anti-inflammatory cytokines, such as IL-10 and TGF-β. These viral activated cells are less sensitive to apoptosis. Moreover, supernatants from ANDV-infected DCs were able to indirectly enhance the permeability of a monolayer of primary HUVEC.Conclusions: Primary human DCs, that are primarily targeted by hantaviruses can productively be infected by ANDV and subsequently induce direct effects favoring a proinflammatory phenotype of infected DCs. Finally, based on our observations, we hypothesize that soluble factors secreted in ANDV-infected DC supernatants, importantly contribute to the endothelial permeability enhancement that characterize the HCPS.

Varicella-zoster virus (VZV) and herpes zoster cause infections of the central nervous system (CNS) manifesting as meningitis or encephalitis. As compared to enterovirus (EV) and herpes simplex virus 1 (HSV-1) and 2 (HSV-2), it is not often tested in CNS infections due to VZV and herpes zoster. There is a certain tendency to think that the findings in the cerebrospinal fluid in infections of the CNS by viruses are comparable among themselves. The exact proportion of patients with VZV primary and reactivation infection who present with lesions prior to or concomitant to its involvement in the CNS is unknown. It is also not known about the risk factors that lead to the reactivation of VZV and CNS involvement. To describe the clinical characteristics and laboratory results of patients with a positive VZV polymerase chain reaction (PCR) and neurological signs and symptoms. A retrospective and descriptive study was performed at the Hospital Universitario de la Pontificia Universidad Católica de Chile (Hospital Clínico UC CHRISTUS) from September 2012 to July 2014. The following parameters were recorded: neurological signs and symptoms, PCR for VZV in cerebrospinal fluid (CSF), comorbidities, personal medical history, cutaneous lesions, CSF characteristics, CNS imaging, electroencephalography (EEG), treatment, mortality, and neurological sequelae. Adult patients with meningitis, encephalitis, or meningoencephalitis due to VZV diagnosed with PCR were included. Out of 70 CSF samples analyzed in the previously mentioned period, 21 cases were VZV positive, 16 cases that had clinical information available were included. The mean age with VZV CNS reactivation was 47 years (range 19-80 years). Five patients (31.25%) were immunocompromised: three had human immunodeficiency virus (HIV), one had kidney transplantation, and one had primary immunodeficiency. Clinical presentation was meningitis in 11 patients (68.75%) and encephalitis in five patients (31.25%). Pleocytosis in CSF was observed in all the samples. The five immunocompromised patients had cutaneous lesions. All patients received antiviral treatment. Therapy duration was from 10 up to 21 days. The clinical course was positive in most patients and the mean hospitalization time was 15 days (range 5-60 days). No mortality was observed. VZV is a worldwide virus and a common cause of CNS infection. The rising incidence is probably due to a better diagnostic method and a frequent clinical suspicion even in the absence of cutaneous lesions, except in immunocompromised cases, as it was observed in the present study. CNS infection presented as a wide spectrum of clinical manifestations with possible neurological sequelae. There was a reduction in neurological morbidity with antiviral therapy. Nonetheless, both the incidence and the morbidity of CNS VZV infection are expected to be diminished by varicella and herpes zoster vaccination. Additionally, there was no increase in mortality in these patients.

Background: Hantavirus cardiopulmonary syndrome (HCPS) has a mortality up to 35–40% and its treatment is mainly supportive. A variable to predict progression from mild to severe disease is unavailable. This study was performed in patients with documented infection by Andes orthohantavirus, and the aim was to find a simple variable to predict progression to moderate/severe HCPS in patients with mild disease at admission. Methods: We performed a retrospective analysis of 175 patients between 2001 and 2018. Patients were categorized into mild, moderate, and severe disease according to organ failure and advanced support need at hospital admission (e.g., mechanical ventilation, vasopressors). Progression to moderate/severe disease was defined accordingly. Clinical and laboratory variables associated with progression were explored. Results: Forty patients with mild disease were identified; 14 of them progressed to moderate/severe disease. Only platelet count was different between those who progressed versus those that did not (37 (34–58) vs. 83 (64–177) K/mm³, p < 0.001). A ROC curve analysis showed an AUC = 0.889 (0.78–1.0) p < 0.001, with a platelet count greater than 115K /mm³ ruling out progression to moderate/severe disease. Conclusions: In patients with mild disease at presentation, platelet count could help to define priority of evacuation to tertiary care centers.

This article focuses on recent developments in knowledge about hantavirus infections and hantavirus cardiopulmonary syndrome in children. We highlight clinical characterization, epidemiology, pathogenesis, diagnostic techniques, and current alternatives for treatment and prevention. After the first description of hantavirus pulmonary syndrome (HPS) in 1993 in the United States, new cases of HPS and new hantavirus species have been described throughout the Americas. The factors involved in the expression of hantavirus disease have, in part, been recognized, but there have been descriptions of newer viruses and newer rodent reservoirs. Several seroprevalence studies suggest that the virus-host interaction has been taking place for many years, and changes in human behavior and wild rodent ecology, sometimes secondary to industrial progress, facilitate the clinical recognition of disease. Sin nombre virus (SNV) and Andes virus (ANDV) are examples of the same disease with differences in the virus virulence and in the host response. The North American syndrome and the Southern HPS differ in epidemiologic patterns and in the spectrum of disease. Currently, no Food and Drug Administration (FDA)-approved antiviral drugs, vaccines, or immunotherapeutic agents are available for treatment of the disease, and therapy is primarily supportive. Intensive care medicine has played an outstanding role in decreasing the lethality of HPS. A ribavirin trial in the United States did not support the use of the drug in fully developed HCPS. Recently published data suggest that a strong neutralizing antibody response may be a predictor of effective clearance of and recovery from SNV infection. This has raised the possibility that passive immunotherapy may be useful in HCPS. Extensive work has been done to develop a hantavirus vaccine, but at present it seems unlikely that a vaccine will be in commercial development in the near future.