Bakgrund: HIV (Human Immunodeficiency Virus) är en sjukdom som påverkar människors immunförsvar. Ca 30–35 miljoner människor lever med HIV i världen. HIV är en sjukdom som påverkar de drabbade både psykiskt och fysiskt. Syfte: Att beskriva vuxna patienters upplevelser av att leva med HIV med fokus på psykiska och fysiska aspekter samt beskriva hur undersökningsgruppen ser ut i de valda artiklarna. Metod: En beskrivande litteraturstudie baserat på 10 vetenskapliga artiklar med kvalitativ ansats. Databasen Cinahl användes till litteratursökningen. Huvudresultat: Resultatet i denna litteraturstudie visade att människor som lever med HIV känner rädsla, depression, oro och stress över att leva med sjukdomen. Känslorna kopplas till upplevelser av stigmatisering och diskriminering från vården och samhället. Människorna som lever med HIV är ofta rädda för hur de blir bemötta av allmänheten. Fysiska symtom som till exempel trötthet påverkar människor som lever med HIV negativt, och förmågan att leva ett normalt liv blir förhindrat. I litteraturstudien presenteras undersökningsgruppen tydligt utifrån vad författarna till de granskade studierna beskrivit. Slutsats: HIV-positiva personer kan mötas i alla vårdinsatser. Känslor av bland annat skuld och skam förekommer ofta hos personer med HIV. Som sjuksköterska är bemötandet av människor med HIV väldigt viktigt. / Background: HIV (Human Immunodeficiency Virus) is a disease that affect the human immune system. Around 30–35 million people are living with HIV in the world. HIV affects people, both mentally and physically. Aim: To describe adults/adult patients experiences of living with HIV, focusing on mental and physical aspects, and to describe how the study group looks in the selected studies. Method: A descriptive literature study, based on 10 scientific articles with qualitative approach. The database that was used to find the articles was Cinahl. Main Results: The result of this literature study shows that people living with HIV daily feel emotions of fear, depression, anxiety and stress due to living with the disease. The emotions connect directly to experiences of stigmatization and discrimination within the healthcare and community. People living with HIV are often afraid how other people will react their disease. Physical symptoms like fatigue affect their everyday life negative, and the ability to live a normal life is prevented. The study group is clearly presented based on what the authors of the audited studies describes. Conclusion: HIV-positive people can be found in all healthcare facilities. Emotions of guilt and shame often occure with people who are living with HIV. As a nurse, the attitude towards people with HIV is very important.

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No advento dos antirretrovirais potentes, os indivíduos infectados pelo vírus da imunodeficiência humana (HIV) começaram a apresentar risco maior para o desenvolvimento de doença cardiovascular (DCV). Este aumento do risco cardiovascular pode ser associado tanto à infecção viral quanto ao tratamento antirretroviral (TARV), que provocam mudanças pró-aterogênicas como o aumento do colesterol total e da lipoproteína de baixa densidade (LDL), além da diminuição da lipoproteína de alta densidade (HDL). A ativação imune e as alterações lipídicas são mecanismos associados com a infecção pelo HIV e com o risco de DCV. Este trabalho utilizou ensaios imunoenzimáticos para a determinação plasmática de biomarcadores emergentes de risco cardiovascular relacionados com modificações da lipoproteína de baixa densidade, a saber: LDL eletronegativa [LDL(-)] e formas oxidadas da LDL, ou seja, LDL-oxi (resíduos lisina da apolipoproteína B100 modificados com malondialdeído), LDL-HNE (resíduos lisina da ApoB100 modificados com 4-hidroxinonenal) e LDL-CML (resíduos lisina da ApoB100 modificados por carboximetila), além de biomarcadores relacionados com a resposta imune-inflamatória, ou seja, autoanticorpos IgG e IgM anti-LDL(-), imunocomplexo de LDL(-) [IC-LDL(-)], proteína amiloide sérica A (SAA) e mieloperoxidase (MPO). Também foram determinadas as concentrações séricas dos biomarcadores de risco relacionados às apolipoproteínas: apolipoproteína A-I (ApoA-I), apolipoproteína B (ApoB) e apolipoproteína E (ApoE). A população estudada incluiu indivíduos com infecção pelo HIV, tratados (HIV-TARV) e não tratados (HIV-NT) com terapia antirretroviral e indivíduos sem infecção pelo HIV (controle). Não foram identificadas diferenças para as concentrações de LDL(-), IC-LDL(-), anti- LDL(-)-IgM, SAA, ApoA-I, ApoB e ApoE entre os grupos estudados (HIV-TARV, HIV-NT e controle). A ApoA-I correlacionou-se positivamente com ApoB e ApoE (rs= 0,418 e rs= 0,347, Spearman, p<0,01) e a ApoB com a ApoE (rs= 0,286, Spearman, p<0,01). Verificou-se correlação inversa entre as concentrações de LDL(-) e IC-LDL(-) (rs= -0,214, Spearman, p<0,05). Os níveis de anti-LDL(-)-IgG correlacionaram-se positivamente com IC-LDL(-) e anti-LDL(-)-IgM (rs= 0,240, Spearman, p<0,05 e rs= 0,348, Spearman, p<0,01). As concentrações de LDL-CML correlacionaram-se positivamente com LDL(-), LDL-oxi, LDL-HNE e IC-LDL(-) (rs= 0,212, Spearman, p<0,05; rs= 0,214, Spearman, p<0,05; rs= 0,573, Spearman, p<0,01 e rs= 0,219, Spearman, p<0,05). O grupo HIV-NT apresentou níveis mais elevados de anticorpos anti-LDL(-)-IgG comparado ao grupo controle (Kruskal-Wallis, p<0,01). Em contraste, observou-se no grupo HIV-NT diminuição das concentrações de MPO, LDL-HNE e LDL-CML em relação ao grupo controle (Kruskal-Wallis, p<0,01). A comparação dos grupos HIV-NT e HIV-TARV demonstrou que o TARV promoveu diminuição das concentrações dos anticorpos anti-LDL(-)-IgG e aumentou os níveis de LDL-oxi (Kruskal-Wallis, p<0,01). O grupo HIV-TARV apresentou aumento das concentrações de LDL-oxi e diminuição dos níveis de MPO, LDL-HNE e LDL-CML em relação ao controle (Kruskal-Wallis, p<0,01). Em conclusão, a infecção pelo HIV modificou o biomarcador de inflamação MPO e o perfil de biomarcadores relacionados às modificações da LDL (menor formação de LDL-HNE e LDL-CML), além aumentar a resposta imune-humoral à LDL eletronegativa [anti-LDL(-)-IgG], enquanto o tratamento com antirretrovirais inibiu esta resposta. Os outros biomarcadores estudados não foram modificados pela infecção viral ou pelo tratamento antirretroviral. / In the advent of potent antiretroviral therapy, individuals infected with human immunodeficiency virus (HIV) have showed an increased risk for developing cardiovascular disease (DCV). Studies have discussed that the increased risk may be related to both the disease and antiretroviral treatment (TARV), that produced pro-atherogenic changes such as increased of total cholesterol and low density lipoprotein (LDL) and decreased high density lipoprotein. The immune activation and the lipid modifications are well known mechanisms related to HIV infection and the risk of DCV. This study used immunoassays for plasma quantification for emerging biomarkers of cardiovascular risk related to modification of low density lipoprotein: electronegative LDL [LDL(-)] and oxidized forms of LDL, LDL-oxi (lysine residues of apolipoprotein B100 modified by malondialdehyde), LDL-HNE (lysine residues of ApoB100 modified by 4-hydroxynonenal) and LDL-CML (lysine residues of ApoB100 modified by carboxymethyl) and biomarkers associated to immune and inflammatory responses, IgG and IgM autoantibodies anti-LDL(-) and immunecomplexe of LDL(-) [IC-LDL(-)], serum amyloid A protein (SAA) and myeloperoxidase (MPO). Also, were determined serum concentrations of risk biomarkers related to apolipoproteins: apolipoprotein A-I (ApoA-I), apolipoprotein B (ApoB) and apolipoprotein E (ApoE). The studied population included patients with HIV infection, treated (HIV-TARV) and untreated (HIV-NT) with antiretroviral therapy and individuals without HIV infection (controle). No differences were identified for concentrations of LDL(-), ICLDL(-), anti-LDL(-)-IgM, SAA, ApoA-I, ApoB and ApoE between studied groups (HIV-TARV, HIV-NT and controle). The ApoA-I was positively correlated to ApoB and ApoE (rs= 0,418 e rs= 0,347, Spearman, p<0,01) and ApoB to ApoE (rs= 0,286, Spearman, p<0,01). There was an inverted correlation between LDL(-) and IC-LDL(-) (rs= -0.214, Spearman, p<0,05). The levels of anti-LDL(-)-IgG were positively correlated to IC-LDL(-) and antibodies anti-LDL(-)-IgM (rs= 0.240; Spearman; p <0.05 and rs= 0.348; Spearman; p <0.01). The concentrations of LDL-CML were positively correlated to LDL(-), LDL-oxi, LDL-HNE e IC-LDL(-) (rs= 0,212, Spearman, p<0,05; rs= 0,214, Spearman, p<0,05; rs= 0,573, Spearman, p<0,01 e rs= 0,219, Spearman, p<0,05). The HIV-NT group showed higher levels of anti-LDL(-)-IgG compared to Control group (Kruskal-Wallis, p<0,01). In contrast, was observed lower levels for HIV-NT group to MPO, LDL-HNE and LDL-CML when compared to Control group (Kruskal-Wallis, p<0,01). The comparison of HIV-NT and HIV-TARV groups demonstrated that TARV caused a decrease of concentrations of anti-LDL(-)-IgG antibodies and an increased of LDL-oxi levels (Kruskal-Wallis, p <0.01). The HIV-TARV group showed increased LDL-oxi concentrations and decreased at levels of MPO, LDL-HNE e LDL-CML when compared to Control (Kruskal-Wallis, p<0,01). In conclusion, the HIV infection changed the biomarker of inflammation MPO and the profile of biomarkers related to modifications of LDL (lower concentrations of LDL-HNE and LDL-CML), as well as increased the humoral-immune response to electronegative LDL [anti-LDL(-)-IgG], while treatment with antiretroviral therapy inhibited this response. The other studied biomarkers were not modified either by viral infection or antiretroviral treatment.

[Truncated abstract] Around 50,000 hip and knee replacements are performed every year in Australia and this number has been increasing by around 13% annually since 1998 (Transplantation Society 2006). The incidence and number of revision surgery has increased by a similar proportion. Autogenous bone or allograft is still the gold standard grafting material and is currently used in a variety of reconstructive surgical procedures. The use of any allograft material carries with it the risk of transfer of disease from donor to recipient. These tissues can transmit the same viral and bacterial infections as blood, and the products of a single donation may be transplanted to several recipients. In contrast to blood, musculoskeletal tissues may come from surgical and cadaveric donation. Overall, the prevention of infection relies on the maintenance of rigid protocols for procurement, donor and allograft testing, secondary sterilisation, and the adherence to internal safety standards within the tissue banks. This thesis aims to determine the risk of viral infection among musculoskeletal tissue donors in Australia. We retrieved and analysed data retrospectively from three large tissue banks in Australia (Perth, Queensland, Victoria). This includes 12,415 musculoskeletal tissue donors, 10,937 of which are surgical donors and 1,478 of which are deceased donors, for the period of 1993 -2004. This data was analysed to determine the prevalence and incidence of viral infections such as human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and human T-lymphotropic virus (HTLV) in musculoskeletal allografts. The results indicate that the risk of viral infection from musculoskeletal tissue transplantation in Australia is low. ... The results indicate that the overall prevalence of screened transfusion-transmitted viral infections did not vary significantly for musculoskeletal donors over the study period, despite falling in the general population and first-time blood donors. In tissue donors, HIV incidence significantly decreased over time, and HBV decreased significantly during 1999-2001; however, there was an apparent increase in the estimated incidence of HCV in 2002-2004 compared with earlier years. Furthermore the residual risk estimate of HIV in the period 2002-2004 has declined 5-fold compared to estimates in the period 1993-1995. This is perhaps due to greater awareness of high risk behaviours among donors, improvement in donor recruitment and an overall decrease in infection levels in the general population. Musculoskeletal tissue is second only to blood as the most frequent transplanted human tissue. Viral infection is a potential complication of tissue transplantation. In this thesis the rates of HIV, HBV, HCV and HTV infection in musculoskeletal donors in Australia were identified and then compared with results in published data from Canada, Scotland and the United States. The study also compared that result with first-time blood donors because they have satisfied similar donor selection criteria (Galea et al. 2006). The results indicate that prevalence and incidence estimates for viral infection in Australian tissue donors are higher than those in blood donors. This was also reported in studies from other countries. Accordingly, it is crucial that viral prevalence and incidence be monitored to evaluate the safety of tissue supply and to improve donor selection processes.

No advento dos antirretrovirais potentes, os indivíduos infectados pelo vírus da imunodeficiência humana (HIV) começaram a apresentar risco maior para o desenvolvimento de doença cardiovascular (DCV). Este aumento do risco cardiovascular pode ser associado tanto à infecção viral quanto ao tratamento antirretroviral (TARV), que provocam mudanças pró-aterogênicas como o aumento do colesterol total e da lipoproteína de baixa densidade (LDL), além da diminuição da lipoproteína de alta densidade (HDL). A ativação imune e as alterações lipídicas são mecanismos associados com a infecção pelo HIV e com o risco de DCV. Este trabalho utilizou ensaios imunoenzimáticos para a determinação plasmática de biomarcadores emergentes de risco cardiovascular relacionados com modificações da lipoproteína de baixa densidade, a saber: LDL eletronegativa [LDL(-)] e formas oxidadas da LDL, ou seja, LDL-oxi (resíduos lisina da apolipoproteína B100 modificados com malondialdeído), LDL-HNE (resíduos lisina da ApoB100 modificados com 4-hidroxinonenal) e LDL-CML (resíduos lisina da ApoB100 modificados por carboximetila), além de biomarcadores relacionados com a resposta imune-inflamatória, ou seja, autoanticorpos IgG e IgM anti-LDL(-), imunocomplexo de LDL(-) [IC-LDL(-)], proteína amiloide sérica A (SAA) e mieloperoxidase (MPO). Também foram determinadas as concentrações séricas dos biomarcadores de risco relacionados às apolipoproteínas: apolipoproteína A-I (ApoA-I), apolipoproteína B (ApoB) e apolipoproteína E (ApoE). A população estudada incluiu indivíduos com infecção pelo HIV, tratados (HIV-TARV) e não tratados (HIV-NT) com terapia antirretroviral e indivíduos sem infecção pelo HIV (controle). Não foram identificadas diferenças para as concentrações de LDL(-), IC-LDL(-), anti- LDL(-)-IgM, SAA, ApoA-I, ApoB e ApoE entre os grupos estudados (HIV-TARV, HIV-NT e controle). A ApoA-I correlacionou-se positivamente com ApoB e ApoE (rs= 0,418 e rs= 0,347, Spearman, p<0,01) e a ApoB com a ApoE (rs= 0,286, Spearman, p<0,01). Verificou-se correlação inversa entre as concentrações de LDL(-) e IC-LDL(-) (rs= -0,214, Spearman, p<0,05). Os níveis de anti-LDL(-)-IgG correlacionaram-se positivamente com IC-LDL(-) e anti-LDL(-)-IgM (rs= 0,240, Spearman, p<0,05 e rs= 0,348, Spearman, p<0,01). As concentrações de LDL-CML correlacionaram-se positivamente com LDL(-), LDL-oxi, LDL-HNE e IC-LDL(-) (rs= 0,212, Spearman, p<0,05; rs= 0,214, Spearman, p<0,05; rs= 0,573, Spearman, p<0,01 e rs= 0,219, Spearman, p<0,05). O grupo HIV-NT apresentou níveis mais elevados de anticorpos anti-LDL(-)-IgG comparado ao grupo controle (Kruskal-Wallis, p<0,01). Em contraste, observou-se no grupo HIV-NT diminuição das concentrações de MPO, LDL-HNE e LDL-CML em relação ao grupo controle (Kruskal-Wallis, p<0,01). A comparação dos grupos HIV-NT e HIV-TARV demonstrou que o TARV promoveu diminuição das concentrações dos anticorpos anti-LDL(-)-IgG e aumentou os níveis de LDL-oxi (Kruskal-Wallis, p<0,01). O grupo HIV-TARV apresentou aumento das concentrações de LDL-oxi e diminuição dos níveis de MPO, LDL-HNE e LDL-CML em relação ao controle (Kruskal-Wallis, p<0,01). Em conclusão, a infecção pelo HIV modificou o biomarcador de inflamação MPO e o perfil de biomarcadores relacionados às modificações da LDL (menor formação de LDL-HNE e LDL-CML), além aumentar a resposta imune-humoral à LDL eletronegativa [anti-LDL(-)-IgG], enquanto o tratamento com antirretrovirais inibiu esta resposta. Os outros biomarcadores estudados não foram modificados pela infecção viral ou pelo tratamento antirretroviral. / In the advent of potent antiretroviral therapy, individuals infected with human immunodeficiency virus (HIV) have showed an increased risk for developing cardiovascular disease (DCV). Studies have discussed that the increased risk may be related to both the disease and antiretroviral treatment (TARV), that produced pro-atherogenic changes such as increased of total cholesterol and low density lipoprotein (LDL) and decreased high density lipoprotein. The immune activation and the lipid modifications are well known mechanisms related to HIV infection and the risk of DCV. This study used immunoassays for plasma quantification for emerging biomarkers of cardiovascular risk related to modification of low density lipoprotein: electronegative LDL [LDL(-)] and oxidized forms of LDL, LDL-oxi (lysine residues of apolipoprotein B100 modified by malondialdehyde), LDL-HNE (lysine residues of ApoB100 modified by 4-hydroxynonenal) and LDL-CML (lysine residues of ApoB100 modified by carboxymethyl) and biomarkers associated to immune and inflammatory responses, IgG and IgM autoantibodies anti-LDL(-) and immunecomplexe of LDL(-) [IC-LDL(-)], serum amyloid A protein (SAA) and myeloperoxidase (MPO). Also, were determined serum concentrations of risk biomarkers related to apolipoproteins: apolipoprotein A-I (ApoA-I), apolipoprotein B (ApoB) and apolipoprotein E (ApoE). The studied population included patients with HIV infection, treated (HIV-TARV) and untreated (HIV-NT) with antiretroviral therapy and individuals without HIV infection (controle). No differences were identified for concentrations of LDL(-), ICLDL(-), anti-LDL(-)-IgM, SAA, ApoA-I, ApoB and ApoE between studied groups (HIV-TARV, HIV-NT and controle). The ApoA-I was positively correlated to ApoB and ApoE (rs= 0,418 e rs= 0,347, Spearman, p<0,01) and ApoB to ApoE (rs= 0,286, Spearman, p<0,01). There was an inverted correlation between LDL(-) and IC-LDL(-) (rs= -0.214, Spearman, p<0,05). The levels of anti-LDL(-)-IgG were positively correlated to IC-LDL(-) and antibodies anti-LDL(-)-IgM (rs= 0.240; Spearman; p <0.05 and rs= 0.348; Spearman; p <0.01). The concentrations of LDL-CML were positively correlated to LDL(-), LDL-oxi, LDL-HNE e IC-LDL(-) (rs= 0,212, Spearman, p<0,05; rs= 0,214, Spearman, p<0,05; rs= 0,573, Spearman, p<0,01 e rs= 0,219, Spearman, p<0,05). The HIV-NT group showed higher levels of anti-LDL(-)-IgG compared to Control group (Kruskal-Wallis, p<0,01). In contrast, was observed lower levels for HIV-NT group to MPO, LDL-HNE and LDL-CML when compared to Control group (Kruskal-Wallis, p<0,01). The comparison of HIV-NT and HIV-TARV groups demonstrated that TARV caused a decrease of concentrations of anti-LDL(-)-IgG antibodies and an increased of LDL-oxi levels (Kruskal-Wallis, p <0.01). The HIV-TARV group showed increased LDL-oxi concentrations and decreased at levels of MPO, LDL-HNE e LDL-CML when compared to Control (Kruskal-Wallis, p<0,01). In conclusion, the HIV infection changed the biomarker of inflammation MPO and the profile of biomarkers related to modifications of LDL (lower concentrations of LDL-HNE and LDL-CML), as well as increased the humoral-immune response to electronegative LDL [anti-LDL(-)-IgG], while treatment with antiretroviral therapy inhibited this response. The other studied biomarkers were not modified either by viral infection or antiretroviral treatment.