Publications by authors named "Sandra Souto"

12 Publications

  • Page 1 of 1

Fear of childbirth in time of the new coronavirus pandemic.

Rev Bras Enferm 2020 13;73(Suppl 2):e20200551. Epub 2020 Nov 13.

Escola Superior de Enfermagem do Porto, Centro de Investigação em Tecnologia e Serviços de Saúde. Porto, Portugal.

Objective: Reflect on how the new coronavirus pandemic triggered or accentuated the fear of childbirth in pregnant women and affected childbirth care practices.

Methods: Reflective analysis of women's pregnancy and childbirth experiences during the current pandemic, supported by the latest scientific evidence and recommendations on the topic.

Results: Pregnancy and childbirth are life-changing events for women, but during the new coronavirus pandemic, fear and uncertainty have taken on an unprecedented dimension in the negative way that many pregnant women have anticipated and experienced childbirth.

Final Considerations: The current period has accentuated a chronic problem: a paternalistic system of health institutions in the approach to childbirth, dense with additional levels of fear in pregnant women. In this context, addressing the fear of childbirth means not giving up the promotion of safe and positive birth experiences for women.
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http://dx.doi.org/10.1590/0034-7167-2020-0551DOI Listing
November 2020

Midwifery interventions to reduce fear of childbirth in pregnant women: a scoping review protocol.

JBI Evid Synth 2020 09;18(9):2045-2057

Nursing School of Porto, Porto, Portugal.

Objective: The objective of the review is to map and analyze midwifery interventions to reduce fear of childbirth in pregnant women.

Introduction: Fear of childbirth is a phenomenon negatively affecting women's health and well-being before and during pregnancy, as well as after childbirth. During the previous few decades, there has been a growing interest in research into interventions to reduce the fear of childbirth in childbearing women. Currently, providing an appropriate model of care for pregnant women with fear of childbirth is a challenge in midwifery care. Therefore, further efforts are needed to identify and examine the characteristics of different midwifery interventions to reduce fear of childbirth in pregnant women.

Inclusion Criteria: This scoping review will consider studies that include interventions to reduce fear of childbirth in pregnant women, led and implemented by midwives, during the antenatal period, in all possible birth scenarios. Quantitative, qualitative, and mixed methods studies will be included.

Methods: The JBI methodology for conducting scoping reviews will be employed. Published and unpublished literature in English, Portuguese, and Spanish, from 1981 to the present, will be included. MEDLINE, CINAHL Complete, Scopus, Web of Science, Embase, and Cochrane Library databases will be searched. Searches for gray literature will be performed. Data will be extracted using a tool developed specifically for the scoping review objectives.
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http://dx.doi.org/10.11124/JBISRIR-D-19-00198DOI Listing
September 2020

Differential immunogene expression profile of European sea bass (Dicentrarchus labrax, L.) in response to highly and low virulent NNV.

Fish Shellfish Immunol 2020 Nov 20;106:56-70. Epub 2020 Jul 20.

Universidad de Málaga, Instituto de Biotecnología y Desarrollo Azul, IBYDA, Departamento de Microbiología, Facultad de Ciencias, 29071, Málaga, Spain. Electronic address:

European sea bass is highly susceptible to the nervous necrosis virus, RGNNV genotype, whereas natural outbreaks caused by the SJNNV genotype have not been recorded. The onset and severity of an infectious disease depend on pathogen virulence factors and the host immune response. The importance of RGNNV capsid protein amino acids 247 and 270 as virulence factors has been previously demonstrated in European sea bass; however, sea bass immune response against nodaviruses with different levels of virulence has been poorly characterized. Knowing the differences between the immune response against both kinds of isolates may be key to get more insight into the host mechanisms responsible for NNV virulence. For this reason, this study analyses the transcription of immunogenes differentially expressed in European sea bass inoculated with nodaviruses with different virulence: a RGNNV virus obtained by reverse genetics (rDl956), highly virulent to sea bass, and a mutated virus (MutDl956, RGNNV virus displaying SJNNV-type amino acids at positions 247 and 270 of the capsid protein), presenting lower virulence. This study has been performed in brain and head kidney, and the main differences between the immunogene responses triggered by both viruses have been observed in brain. The immunogene response in this organ is stronger after inoculation with the most virulent virus, and the main differences involved genes related with IFN I system, inflammatory response, cell-mediated response, and apoptosis. The lower virulence of MutDl956 to European sea bass can be associated with a delayed IFN I response, as well as an early and transitory inflammation and cell-mediated responses, suggesting that those can be pivotal elements in controlling the viral infection, and therefore, their functional activity could be analysed in future studies. In addition, this study supports the role of capsid amino acids at positions 247 and 270 as important determinants of RGNNV virulence to European sea bass.
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http://dx.doi.org/10.1016/j.fsi.2020.06.052DOI Listing
November 2020

Betanodavirus and VER Disease: A 30-year Research Review.

Pathogens 2020 Feb 9;9(2). Epub 2020 Feb 9.

Departamento de Microbioloxía e Parasitoloxía-Instituto de Acuicultura. Universidade de Santiago de Compostela. 15782 Santiago de Compostela, Spain.

The outbreaks of viral encephalopathy and retinopathy (VER), caused by nervous necrosis virus (NNV), represent one of the main infectious threats for marine aquaculture worldwide. Since the first description of the disease at the end of the 1980s, a considerable amount of research has gone into understanding the mechanisms involved in fish infection, developing reliable diagnostic methods, and control measures, and several comprehensive reviews have been published to date. This review focuses on host-virus interaction and epidemiological aspects, comprising viral distribution and transmission as well as the continuously increasing host range (177 susceptible marine species and epizootic outbreaks reported in 62 of them), with special emphasis on genotypes and the effect of global warming on NNV infection, but also including the latest findings in the NNV life cycle and virulence as well as diagnostic methods and VER disease control.
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http://dx.doi.org/10.3390/pathogens9020106DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7168202PMC
February 2020

Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass.

Sci Rep 2019 Oct 1;9(1):14068. Epub 2019 Oct 1.

Universidad de Málaga, Departamento de Microbiología, Málaga, Spain.

European sea bass (Dicentrarchus labrax) is severely affected by nervous necrosis disease, caused by nervous necrosis virus (NNV). Two out of the four genotypes of this virus (red-spotted grouper nervous necrosis virus, RGNNV; and striped jack nervous necrosis virus, SJNNV) have been detected in sea bass, although showing different levels of virulence to this fish species. Thus, sea bass is highly susceptible to RGNNV, whereas outbreaks caused by SJNNV have not been reported in this fish species. The role of the capsid protein (Cp) amino acids 247 and 270 in the virulence of a RGNNV isolate to sea bass has been evaluated by the generation of recombinant RGNNV viruses harbouring SJNNV-type amino acids in the above mentioned positions (Mut247Dl965, Mut270Dl965 and Mut247 + 270Dl965). Viral in vitro and in vivo replication, virus virulence and fish immune response triggered by these viruses have been analysed. Mutated viruses replicated on E-11 cells, although showing some differences compared to the wild type virus, suggesting that the mutations can affect the viral cell recognition and entry. In vivo, fish mortality caused by mutated viruses was 75% lower, and viral replication in sea bass brain was altered compared to non-mutated virus. Regarding sea bass immune response, mutated viruses triggered a lower induction of IFN I system and inflammatory response-related genes. Furthermore, mutations caused changes in viral serological properties (especially the mutation in amino acid 270), inducing higher seroconversion and changing antigen recognition.
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http://dx.doi.org/10.1038/s41598-019-50622-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6773868PMC
October 2019

Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase.

Vet Res 2019 Jun 21;50(1):50. Epub 2019 Jun 21.

Instituto de Acuicultura, Departamento de Microbiología y Parasitología-Universidade de Santiago de Compostela, 15706, Santiago de Compostela, Spain.

Nervous necrosis virus (NNV), Genus Betanodavirus, is the causative agent of viral encephalopathy and retinopathy (VER), a neuropathological disease that causes fish mortalities worldwide. The NNV genome is composed of two single-stranded RNA molecules, RNA1 and RNA2, encoding the RNA polymerase and the coat protein, respectively. Betanodaviruses are classified into four genotypes: red-spotted grouper nervous necrosis virus (RGNNV), striped jack nervous necrosis virus (SJNNV), barfin flounder nervous necrosis virus (BFNNV) and tiger puffer nervous necrosis virus (TPNNV). In Southern Europe the presence of RGNNV, SJNNV and their natural reassortants (in both RNA1/RNA2 forms: RGNNV/SJNNV and SJNNV/RGNNV) has been reported. Pathology caused by these genotypes is closely linked to water temperature and the RNA1 segment encoding amino acids 1-445 has been postulated to regulate viral adaptation to temperature. Reassortants isolated from sole (RGNNV/SJNNV) show 6 substitutions in this region when compared with the RGNNV genotype (positions 41, 48, 218, 223, 238 and 289). We have demonstrated that change of these positions to those present in the RGNNV genotype cause low and delayed replication in vitro when compared with that of the wild type strain at 25 and 30 °C. The experimental infections confirmed the impact of the mutations on viral replication because at 25 °C the viral load and the mortality were significantly lower in fish infected with the mutant than in those challenged with the non-mutated virus. It was not possible to challenge fish at 30 °C because of the scarce tolerance of sole to this temperature.
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http://dx.doi.org/10.1186/s13567-019-0669-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6588924PMC
June 2019

Amino acid changes in the capsid protein of a reassortant betanodavirus strain: Effect on viral replication in vitro and in vivo.

J Fish Dis 2019 Feb 3;42(2):221-227. Epub 2018 Dec 3.

Departamento de Microbiología y Parasitología, Instituto de Acuicultura, Universidade de Santiago de Compostela, Santiago de Compostela, Spain.

Betanodavirus reassortant strains (RGNNV/SJNNV) isolated from Senegalese sole harbour an SJNNV capsid featuring several changes with respect to the SJNNV-type strain, sharing three hallmark substitutions. Here, we have employed recombinant strains harbouring mutations in these positions (r20 and r20 + 247 + 270) and have demonstrated that the three substitutions affect different steps of the viral replication process. Adsorption ability and efficiency of viral attachment were only affected by substitutions in the C-terminal side of the capsid. However, the concurrent mutation in the N-terminal side seems to slightly decrease these properties, suggesting that this region could also be involved in viral binding. Differences in the intracellular and extracellular production of the mutant strains suggest that both the C-terminal and N-terminal regions of the capsid protein may be involved in the particle budding. Furthermore, viral replication in sole brain tissue of the mutant strains, and especially double- and triple-mutant strains, is clearly delayed with respect to the wt strain. These data support previous findings indicating that the C-terminal side plays a role in virulence because of a slower spread in the fish host brain and suggest that the concurrent participation of the N-terminal side is also important for viral replication in vivo.
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http://dx.doi.org/10.1111/jfd.12916DOI Listing
February 2019

Betanodavirus infection in primary neuron cultures from sole.

Vet Res 2018 Sep 5;49(1):86. Epub 2018 Sep 5.

Departamento de Microbiología y Parasitología, Instituto de Acuicultura, Universidade de Santiago de Compostela, 15706, Santiago de Compostela, Spain.

Nervous necrosis virus (NNV), G. Betanodavirus, is the causative agent of viral encephalopathy and retinopathy, a disease that causes mass mortalities in a wide range of fish species. Betanodaviruses are neurotropic viruses and their replication in the susceptible fish species seems to be almost entirely restricted to nerve tissue. However, none of the cell lines used for NNV propagation has a nervous origin. In this study, first we established a protocol for the primary culture of neurons from Senegalese sole, which made it possible to further study virus-host cell interactions. Then, we compared the replication of three NNV strains with different genotypes (SJNNV, RGNNV and a RGNNV/SJNNV reassortant strain) in sole neuron primary cultures and E-11 cells. In addition, to study how two amino acid substitutions at the c-terminal of the capsid protein (positions 247 and 270) affect the binding to cell receptors, a recombinant strain was also tested. The results show that sole neural cells enabled replication of all the tested NNV strains. However, the recombinant strain shows a clearly delayed replication when compared with the wt strain. This delay was not observed in virus replicating in E-11 cells, suggesting a viral interaction with different cell receptors. The establishment of a sole primary neuronal culture protocol provides an important tool for research into betanodavirus infection in sole.
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http://dx.doi.org/10.1186/s13567-018-0580-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6125867PMC
September 2018

Modification of betanodavirus virulence by substitutions in the 3' terminal region of RNA2.

J Gen Virol 2018 09 24;99(9):1210-1220. Epub 2018 Jul 24.

1​Departamento de Microbiología y Parasitología, Instituto de Acuicultura, Universidade de Santiago de Compostela, 15706 Santiago de Compostela, Spain.

Betanodaviruses have bi-segmented positive-sense RNA genomes, consisting of RNAs 1 and 2. For some members of the related genus alphanodavirus, the 3' terminal 50 nucleotides (nt) of RNA2, including a predicted stem-loop structure (3'SL), are essential for replication. We investigate the possible existence and role of a similar structure in a reassortant betanodavirus strain (RGNNV/SJNNV). In this study, we developed three recombinant strains containing nucleotide changes at positions 1408 and 1412. Predictive models showed stem-loop structures involving nt 1398-1421 of the natural reassortant whereas this structure is modified in the recombinant viruses harbouring point mutations r1408 and r1408-1412, but not in r1412. Results obtained from infectivity assays showed differences between the reference strains and the mutants in both RNA1 and RNA2 synthesis. Moreover, an imbalance between the synthesis of both segments was demonstrated, mainly with the double mutant. All these results suggest an interaction between RNA1 and the 3' non-coding regions (3'NCR) of RNA2. In addition, the significant attenuation of the virulence for Senegalese sole and the delayed replication of r1408-1412 in brain tissues may point to an interaction of RNA2 with host cellular proteins.
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http://dx.doi.org/10.1099/jgv.0.001112DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6230769PMC
September 2018

Betanodavirus infection in bath-challenged Solea senegalensis juveniles: A comparative analysis of RGNNV, SJNNV and reassortant strains.

J Fish Dis 2018 Oct 20;41(10):1571-1578. Epub 2018 Jul 20.

Departamento de Microbiología y Parasitología, Instituto de Acuicultura, Universidade de Santiago de Compostela, Santiago de Compostela, Spain.

Senegalese sole has been shown to be highly susceptible to betanodavirus infection, although virulence differences were observed between strains. To study the mechanisms involved in these differences, we have analysed the replication in brain tissue of three strains with different genotypes during 15 days after bath infection. In addition, possible portals of entry for betanodavirus into sole were investigated. The reassortant RGNNV/SJNNV and the SJNNV strain reached the brain after 1 and 2 days postinfection, respectively. Although no RGNNV replication was detected until day 3-4 postinfection, at the end of the experiment this strain yielded the highest viral load; this is in accordance with previous studies in which sole infected with the reassortant showed more acute signs and earlier mortality than the RGNNV and SJNNV strains. Differences between strains were also observed in the possible portals of entry. Thus, whereas the reassortant strain could infect sole mainly through the skin or the oral route, and, to a minor extent, through the gills, the SJNNV strain seems to enter fish only through the gills and the RGNNV strain could use all tissues indistinctly. Taken together, all these results support the hypothesis that reassortment has improved betanodavirus infectivity for sole.
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http://dx.doi.org/10.1111/jfd.12865DOI Listing
October 2018

Influence of temperature on Betanodavirus infection in Senegalese sole (Solea senegalensis).

Vet Microbiol 2015 Sep 8;179(3-4):162-7. Epub 2015 Jul 8.

Universidad de Santiago de Compostela, Departamento de Microbiología y Parasitología, Instituto de Acuicultura, Constantino Candeira, Santiago de Compostela, A Coruña CP-15705, Spain.

In this study Senegalese sole juveniles were experimentally infected with a reassortant Betanodavirus strain at three different temperatures: 22 °C, 18 °C and 16 °C by bath challenge and cohabitation. The results obtained showed that virus virulence decreased by reducing the water temperature. At 22 °C mortalities reached 100%, at 18 °C they ranged from 75 to 80% and at 16 °C only 8% of the fish died. In addition, horizontal transmission was demonstrated regardless of the rearing temperature. At 16 °C active viral replication was detected up to 66 days post-infection, but no signs of the disease were observed and only a very low level of mortality was recorded. The increase in water temperature from 16 to 22 °C caused a quick rise in the viral load and a subsequent outbreak of mortalities. These findings demonstrate that this reassortant Betanodavirus strain can cause a persistent infection in Senegalese sole at low temperatures (16 °C) for long periods of time, and when temperature increases the virus is able to trigger an acute infection and provoke high mortalities.
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http://dx.doi.org/10.1016/j.vetmic.2015.07.004DOI Listing
September 2015

In vitro and in vivo characterization of molecular determinants of virulence in reassortant betanodavirus.

J Gen Virol 2015 Jun 27;96(Pt 6):1287-1296. Epub 2015 Jan 27.

Instituto de Acuicultura, Universidad de Santiago de Compostela, A Coruña, Spain.

We previously reported that betanodavirus reassortant strains [redspotted grouper nervous necrosis virus/striped jack nervous necrosis virus (SJNNV)] isolated from Senegalese sole (Solea senegalensis) exhibited a modified SJNNV capsid amino acid sequence, with changes at aa 247 and 270. In the current study, we investigated the possible role of both residues as putative virulence determinants. Three recombinant viruses harbouring site-specific mutations in the capsid protein sequence, rSs160.03247 (S247A), rSs160.03270 (S270N) and rSs160.03247+270 (S247A/S270N), were generated using a reverse genetics system. These recombinant viruses were studied in cell culture and in vivo in the natural fish host. The three mutant viruses were shown to be infectious and able to replicate in E-11 cells, reaching final titres similar to the WT virus, although with a somewhat slower kinetics of replication. When the effect of the amino acid substitutions on virus pathogenicity was evaluated in Senegalese sole, typical clinical signs of betanodavirus infection were observed in all groups. However, fish mortality induced by all three mutant viruses was clearly affected. Roughly 40 % of the fish survived in these three groups in contrast with the WT virus which killed 100 % of the fish. These data demonstrated that aa 247 and 270 play a major role in betanodavirus virulence although when both mutated aa 247 and 270 are present, corresponding recombinant virus was not further attenuated.
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http://dx.doi.org/10.1099/vir.0.000064DOI Listing
June 2015