-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
*The professional part involved in this article is only for medical professionals to read as a reference to explore the reasons why HIV-infected people live less healthily
.
In the process of aging, people’s ability to cope with stress factors decreases and the level of inflammation increases, but this inflammation is chronic, low-level and asymptomatic, not caused by infection, and it will accelerate aging and age-related diseases.
Development, this condition is called "inflammatory aging"
.
In addition to healthy people, inflammatory senescence in patients with chronic diseases requires special attention, for example, people infected with human immunodeficiency virus (HIV)
.
The emergence of antiretroviral therapy (ART) has made HIV infection a controllable chronic disease, and it has also significantly increased the life expectancy of HIV-infected patients
.
Among the infected persons who started ART when the CD4 cell count was ≥500 cells/μL, there was almost no difference in life expectancy from healthy persons [1], but their healthy life span was 9-10 years shorter than that, causing this gap One of the important factors is the increased risk of age-related diseases, that is, the development of inflammatory aging [1]
.
Therefore, more and more ART studies have taken into account the elderly infected people, hoping that a new generation of treatment programs can give them a better treatment experience
.
Not long ago, the results of a Phase IIIb clinical trial were published.
This trial included people 65 years of age and older who were receiving Averevir/Colbisstat/ Emtricitabine/Profol Tenofovir (EVG/c /FTC/TAF) or tenofovir disoproxil fumarate (TDF)-based treatment regimens that achieve virological suppression after infection
.
The test results showed that after switching to Biktegravir/emtricitabine/Profenofovir (B/F/TAF), their virological suppression was sustained and tolerated during the 48-week test period Good sex, improved treatment satisfaction, and no decline in the quality of healthy life [2]
.
The results of a meta-analysis of 4 international studies including this trial [3] announced at the International AIDS Conference in 2020 (AIDS 2020) are consistent with the individual results of this trial
.
Figure 1: 48 weeks after conversion to B/F/TAF, all participants with virological data maintained virological suppression.
HIV-infected persons as a special population with immune system defects, how to restore the normal number of immune cells and immune system Function and reducing inflammation have always been a major issue in the comprehensive management of HIV infection.
For them, does inflammatory aging increase the risk of age-related diseases? In the process of long-term disease management, what methods may be able to resist inflammatory aging? 01 Discussion on the mechanism of inflammatory aging To explore these two issues, we must first understand the inflammatory mechanism that accompanies aging
.
Although the current understanding of the mechanism of inflammatory aging cannot be said to be fully grasped, there have been some findings, which can be divided into three categories: increased release of inflammatory cytokines from senescence-related cells, immune remodeling, and intestinal microbial development.
Change
.
Next, we will introduce them one by one
.
In the process of body aging, there will be a large number of senescent cells, mainly including fibroblasts and endothelial cells.
They are a special type of cells that are "old but not dead", do not proliferate, and do not normally apoptotic, and they have also cultivated " Senescence-associated secretory phenotype (SASP)" can secrete cytokines that promote fibrosis and inflammation [4]
.
In addition to senescent cells, adipocytes are also an important source of inflammatory cytokines.
Many studies have found that obesity is related to increased levels of inflammation [5], and free fatty acids stored and released by adipose tissue can promote macrophages, etc.
The activation of immune cells also increases the level of inflammatory cytokines
.
Next is immune remodeling.
Immune remodeling related to aging is called "immune aging".
Both innate immunity and adaptive immunity will change during the aging process, which manifests itself in many types, such as monocytes in innate immune cells.
Phagocytosis is impaired, and the formation of extracellular traps of neutrophils is reduced [6-7], and extracellular traps are a way for neutrophils to capture and kill pathogens, increasing the risk of viral and bacterial infections during aging
.
In terms of adaptive immunity, there may be a decrease in naive T cells and a decrease in the ratio of CD4/CD8 [8].
The decrease in the ratio of CD4/CD8 is also a very serious problem in HIV-infected patients.
It is a manifestation of impaired immune function and higher inflammation.
Level related
.
In addition, there are changes in intestinal microbes[9].
The diversity of intestinal microbes decreases with age, and the structure of microbes changes.
The bacteria that produce short-chain fatty acids that inhibit inflammation decrease, and the level of inflammation increases, which will also lead to the intestinal barrier.
Damaged, microbes translocate, and further promote systemic inflammation
.
Figure 2: The mechanism of inflammatory senescence in HIV-infected persons 02 The effect of HIV infection on inflammatory senescence For HIV-infected persons, these mechanisms may have a superimposed effect on HIV infection and further promote the development of inflammatory senescence, such as the one just mentioned Immune aging is more serious in HIV-infected people
.
Infected patients usually have more effector T cells and terminally differentiated memory T cells, which is evidence of immune activation [10]
.
Their peripheral blood is enriched with T cells with immune senescence phenotype, which is related to aging and many adverse clinical outcomes of HIV infection [11-12]
.
In addition, there are a large number of failed HIV-specific T cells, high expression of PD-1 [13], and the co-existence of many pro-inflammatory immune cells that together lead to immune disorders in virologically suppressed infected persons receiving ART
.
In addition to the above-mentioned immune regulation effects, HIV infection can also deplete IL-17-producing helper T cells, which can produce cytokines that enhance the tight junctions of intestinal epithelial cells, and their depletion can lead to damage to the intestinal barrier [ 14], aggravate the translocation of intestinal microbes
.
Picture from Pixabay.
com Not only HIV infection itself, ART drugs are also related to the development of aging and inflammation, such as some protease inhibitors (PI), nucleoside reverse transcriptase inhibitors (NRTI) and non-nucleoside reverse Recording enzyme inhibitor (NNRTI) is related to mitochondrial dysfunction, which is an important factor in cellular senescence and SASP
.
An in vitro study has shown that the ART combination of 2 NRTI, 2 NRTI+PI, and 2 NRTI+2 PI will increase the level of reactive oxygen species (ROS) of neural progenitor cells and accelerate cell senescence [15]
.
Early studies have shown that integrase inhibitors (INSTI) and CCR5 antagonists are unlikely to have these adverse effects [16-17]
.
There are also some ART drugs that can cause large changes in lipid levels.
The increase in subcutaneous fat in HIV-infected patients is related to the increase in the level of systemic inflammation markers
.
Their dyslipidemia, especially the increase in oxidized low-density lipoprotein cholesterol, will promote the formation of pro-inflammatory foam cells in the blood vessels, which is related to systemic inflammation [18-19]
.
At present, in order to reduce the drug burden and adverse events of HIV-infected patients, studies have supported the use of dual therapy to replace the widely used triple therapy.
However, dual therapy has encountered some challenges in terms of inflammation
.
At this year's Conference on Retroviruses and Opportunistic Infections (CROI), the results of a subgroup analysis of 148 infected persons in the Spanish AIDS Research Network (CoRIS) were published
.
The CoRIS cohort explored the changes in virological outcomes and inflammatory markers of infected patients who achieved virological suppression after triple therapy treatment, continued triple therapy or switched to dual or monotherapy, and we also conducted other research results based on it.
After the interpretation, interested readers can click here to review
.
In infected patients who continue to use triple therapy, in long-term observation, the levels of inflammation markers interleukin-6 (IL-6), C-reactive protein (CRP) and D-dimer gradually decrease, and the triple therapy is switched to two The number of combination therapy is gradually increasing, and this increase is directly related to dual therapy
.
Compared with the triple therapy group, dual therapy is associated with increased risk of CRP (aOR=3.
3, 95%CI 1.
1-10) and D-dimer (aOR=3.
7, 95%CI 1.
1-13) [20 ]
.
Figure 3: The changes of IL-6, CPR and D-dimer levels in the two groups of infected persons with triple therapy (blue) and double therapy (red) over time (click to view larger image) currently assessing the effects of dual therapy on inflammation There are not enough studies on the impact, and the results are not completely consistent.
Many studies only focused on the changes in inflammatory markers, and did not explore the inhibitory effect of T cell activation, indicating that the effect of dual therapy on inflammation is not clear, and the changes in inflammatory markers The heterogeneity of the research also needs to be studied in depth
.
03Management of inflammatory senescence in HIV-infected persons Faced with such a complicated mechanism, what can we do to combat inflammatory senescence in HIV-infected persons? First of all, it is necessary to change bad life>
.
Second, intervene in mental health.
Subclinical depression and anxiety are common in HIV-infected people.
Mental stress can significantly increase the production of various inflammatory markers such as IL-6 and tumor necrosis factor-α (TNF-α).
Intervention and regulation of it helps to reduce the level of inflammation [25]
.
In addition, it is necessary to strengthen social support.
HIV-infected people are full of more uncertainties about aging.
Supportive social bonds can improve their physical function and mental health, improve treatment compliance, and are an important auxiliary means of HIV management
.
Third, to optimize the ART program, individualized program recommendations should be considered for the actual situation of the infected person
.
For example, as people get older, the liver and kidney metabolism of some drugs decreases.
At the same dose, exposure to drug concentrations and adverse reactions may increase, and inflammation-related mechanisms may promote inflammatory aging.
Therefore, adverse reactions should be closely monitored.
, Adjust the drug dosage or program in time
.
For example, as we mentioned at the beginning, after the elderly infected with B/F/TAF are converted to B/F/TAF, while maintaining virological suppression, it can improve treatment satisfaction and at the same time ensure the healthy quality of life of the elderly infected
.
Moreover, as mentioned earlier, during the aging process, HIV-infected senescent cells in mitochondrial dysfunction and changes in lipid metabolism lead to increased inflammation.
They need new drugs that have less impact on mitochondrial function and lipid levels, such as new drugs.
Generation INSTI
.
The picture is from veer.
com.
Fourth, to improve the composition of intestinal microbes.
Studies have found that probiotics can improve intestinal homeostasis and reduce inflammation in HIV-infected patients receiving ART [26-27].
The pilot study also showed neurological recognition.
Knowing the outcome of improvement, therefore, supplementing with probiotics to improve intestinal microbes may have clinical benefits [28-29]
.
Fifth, auxiliary anti-inflammatory and anti-aging drugs, including IL-1b or IL-6 inhibitors, as well as metformin, statins and senolytics
.
The first two target key molecules in the development of inflammation, and reduce the level of inflammation by blocking the inflammatory pathway
.
Statins are commonly used drugs for the elderly and may have the added benefit of reducing vascular and systemic inflammation
.
SATURN-HIV research has proved that rosuvastatin is related to reducing the activation of monocytes/macrophages in HIV-infected patients [30]
.
Metformin can reduce inflammatory factors, improve intestinal microbes, increase short-chain fatty acids, and reduce inflammation levels
.
Senolytics is the general term for a new class of drugs, that is, drugs that directly target and eliminate those "old but not dead" senescent cells [31]
.
In general, inflammation occurs with age and is the basis of many age-related diseases.
There are multiple mechanisms that work together.
Even HIV-infected people who insist on ART treatment are easily affected by it
.
In the future, there is much we can do in this regard, including continuing to explore the mechanism of inflammatory aging; developing new ART drugs that help inhibit inflammation, improving existing drug regimens or drug combinations; improving comprehensive disease management and increasing Comprehensive assessment of psychological, life obstacles, physical changes and drug interactions, and multilateral interventions
.
In addition, in terms of clinical research, older HIV-infected people are usually excluded from early trials.
Increasing clinical research focusing on them as the main research object will help to develop a more realistic situation for elderly HIV-infected people.
Treatment options
.
Through these improvements and efforts, greater progress will be made in extending the life expectancy and healthy life of HIV-infected persons and improving their quality of life in the future
.
Rosuvastatin reduces vascular inflammation and T cell and monocyte activation in HIV-infected subjects on antiretroviral therapy[J].
Journal of acquired immune deficiency syndromes (1999), 2015, 68(4): 396.
[31] Hickson LTJ, Prata LGPL, Bobart SA, et al.
Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease[J].
EBioMedicine, 2019, 47: 446-456.
How to manage the barriers to knowledge? Experts say so! Get more latest literature, guidelines and cutting-edge information in the fields of infectious diseases, hepatitis and AIDS-welcome to follow "Jizhiyi"-"This article is only used to provide scientific information to medical and health professionals, and does not represent the platform's position" Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease[J].
EBioMedicine, 2019, 47: 446-456.
A wonderful review of how to manage HIV-related cognitive impairment? Experts say so! Get more latest literature, guidelines and cutting-edge information in the fields of infectious diseases, hepatitis and AIDS-welcome to follow "Jizhiyi"-"This article is only used to provide scientific information to medical and health professionals, and does not represent the platform's position" Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease[J].
EBioMedicine, 2019, 47: 446-456.
A wonderful review of how to manage HIV-related cognitive impairment? Experts say so! Get more latest literature, guidelines and cutting-edge information in the fields of infectious diseases, hepatitis and AIDS-welcome to follow "Jizhiyi"-"This article is only used to provide scientific information to medical and health professionals, and does not represent the platform's position"
.
In the process of aging, people’s ability to cope with stress factors decreases and the level of inflammation increases, but this inflammation is chronic, low-level and asymptomatic, not caused by infection, and it will accelerate aging and age-related diseases.
Development, this condition is called "inflammatory aging"
.
In addition to healthy people, inflammatory senescence in patients with chronic diseases requires special attention, for example, people infected with human immunodeficiency virus (HIV)
.
The emergence of antiretroviral therapy (ART) has made HIV infection a controllable chronic disease, and it has also significantly increased the life expectancy of HIV-infected patients
.
Among the infected persons who started ART when the CD4 cell count was ≥500 cells/μL, there was almost no difference in life expectancy from healthy persons [1], but their healthy life span was 9-10 years shorter than that, causing this gap One of the important factors is the increased risk of age-related diseases, that is, the development of inflammatory aging [1]
.
Therefore, more and more ART studies have taken into account the elderly infected people, hoping that a new generation of treatment programs can give them a better treatment experience
.
Not long ago, the results of a Phase IIIb clinical trial were published.
This trial included people 65 years of age and older who were receiving Averevir/Colbisstat/ Emtricitabine/Profol Tenofovir (EVG/c /FTC/TAF) or tenofovir disoproxil fumarate (TDF)-based treatment regimens that achieve virological suppression after infection
.
The test results showed that after switching to Biktegravir/emtricitabine/Profenofovir (B/F/TAF), their virological suppression was sustained and tolerated during the 48-week test period Good sex, improved treatment satisfaction, and no decline in the quality of healthy life [2]
.
The results of a meta-analysis of 4 international studies including this trial [3] announced at the International AIDS Conference in 2020 (AIDS 2020) are consistent with the individual results of this trial
.
Figure 1: 48 weeks after conversion to B/F/TAF, all participants with virological data maintained virological suppression.
HIV-infected persons as a special population with immune system defects, how to restore the normal number of immune cells and immune system Function and reducing inflammation have always been a major issue in the comprehensive management of HIV infection.
For them, does inflammatory aging increase the risk of age-related diseases? In the process of long-term disease management, what methods may be able to resist inflammatory aging? 01 Discussion on the mechanism of inflammatory aging To explore these two issues, we must first understand the inflammatory mechanism that accompanies aging
.
Although the current understanding of the mechanism of inflammatory aging cannot be said to be fully grasped, there have been some findings, which can be divided into three categories: increased release of inflammatory cytokines from senescence-related cells, immune remodeling, and intestinal microbial development.
Change
.
Next, we will introduce them one by one
.
In the process of body aging, there will be a large number of senescent cells, mainly including fibroblasts and endothelial cells.
They are a special type of cells that are "old but not dead", do not proliferate, and do not normally apoptotic, and they have also cultivated " Senescence-associated secretory phenotype (SASP)" can secrete cytokines that promote fibrosis and inflammation [4]
.
In addition to senescent cells, adipocytes are also an important source of inflammatory cytokines.
Many studies have found that obesity is related to increased levels of inflammation [5], and free fatty acids stored and released by adipose tissue can promote macrophages, etc.
The activation of immune cells also increases the level of inflammatory cytokines
.
Next is immune remodeling.
Immune remodeling related to aging is called "immune aging".
Both innate immunity and adaptive immunity will change during the aging process, which manifests itself in many types, such as monocytes in innate immune cells.
Phagocytosis is impaired, and the formation of extracellular traps of neutrophils is reduced [6-7], and extracellular traps are a way for neutrophils to capture and kill pathogens, increasing the risk of viral and bacterial infections during aging
.
In terms of adaptive immunity, there may be a decrease in naive T cells and a decrease in the ratio of CD4/CD8 [8].
The decrease in the ratio of CD4/CD8 is also a very serious problem in HIV-infected patients.
It is a manifestation of impaired immune function and higher inflammation.
Level related
.
In addition, there are changes in intestinal microbes[9].
The diversity of intestinal microbes decreases with age, and the structure of microbes changes.
The bacteria that produce short-chain fatty acids that inhibit inflammation decrease, and the level of inflammation increases, which will also lead to the intestinal barrier.
Damaged, microbes translocate, and further promote systemic inflammation
.
Figure 2: The mechanism of inflammatory senescence in HIV-infected persons 02 The effect of HIV infection on inflammatory senescence For HIV-infected persons, these mechanisms may have a superimposed effect on HIV infection and further promote the development of inflammatory senescence, such as the one just mentioned Immune aging is more serious in HIV-infected people
.
Infected patients usually have more effector T cells and terminally differentiated memory T cells, which is evidence of immune activation [10]
.
Their peripheral blood is enriched with T cells with immune senescence phenotype, which is related to aging and many adverse clinical outcomes of HIV infection [11-12]
.
In addition, there are a large number of failed HIV-specific T cells, high expression of PD-1 [13], and the co-existence of many pro-inflammatory immune cells that together lead to immune disorders in virologically suppressed infected persons receiving ART
.
In addition to the above-mentioned immune regulation effects, HIV infection can also deplete IL-17-producing helper T cells, which can produce cytokines that enhance the tight junctions of intestinal epithelial cells, and their depletion can lead to damage to the intestinal barrier [ 14], aggravate the translocation of intestinal microbes
.
Picture from Pixabay.
com Not only HIV infection itself, ART drugs are also related to the development of aging and inflammation, such as some protease inhibitors (PI), nucleoside reverse transcriptase inhibitors (NRTI) and non-nucleoside reverse Recording enzyme inhibitor (NNRTI) is related to mitochondrial dysfunction, which is an important factor in cellular senescence and SASP
.
An in vitro study has shown that the ART combination of 2 NRTI, 2 NRTI+PI, and 2 NRTI+2 PI will increase the level of reactive oxygen species (ROS) of neural progenitor cells and accelerate cell senescence [15]
.
Early studies have shown that integrase inhibitors (INSTI) and CCR5 antagonists are unlikely to have these adverse effects [16-17]
.
There are also some ART drugs that can cause large changes in lipid levels.
The increase in subcutaneous fat in HIV-infected patients is related to the increase in the level of systemic inflammation markers
.
Their dyslipidemia, especially the increase in oxidized low-density lipoprotein cholesterol, will promote the formation of pro-inflammatory foam cells in the blood vessels, which is related to systemic inflammation [18-19]
.
At present, in order to reduce the drug burden and adverse events of HIV-infected patients, studies have supported the use of dual therapy to replace the widely used triple therapy.
However, dual therapy has encountered some challenges in terms of inflammation
.
At this year's Conference on Retroviruses and Opportunistic Infections (CROI), the results of a subgroup analysis of 148 infected persons in the Spanish AIDS Research Network (CoRIS) were published
.
The CoRIS cohort explored the changes in virological outcomes and inflammatory markers of infected patients who achieved virological suppression after triple therapy treatment, continued triple therapy or switched to dual or monotherapy, and we also conducted other research results based on it.
After the interpretation, interested readers can click here to review
.
In infected patients who continue to use triple therapy, in long-term observation, the levels of inflammation markers interleukin-6 (IL-6), C-reactive protein (CRP) and D-dimer gradually decrease, and the triple therapy is switched to two The number of combination therapy is gradually increasing, and this increase is directly related to dual therapy
.
Compared with the triple therapy group, dual therapy is associated with increased risk of CRP (aOR=3.
3, 95%CI 1.
1-10) and D-dimer (aOR=3.
7, 95%CI 1.
1-13) [20 ]
.
Figure 3: The changes of IL-6, CPR and D-dimer levels in the two groups of infected persons with triple therapy (blue) and double therapy (red) over time (click to view larger image) currently assessing the effects of dual therapy on inflammation There are not enough studies on the impact, and the results are not completely consistent.
Many studies only focused on the changes in inflammatory markers, and did not explore the inhibitory effect of T cell activation, indicating that the effect of dual therapy on inflammation is not clear, and the changes in inflammatory markers The heterogeneity of the research also needs to be studied in depth
.
03Management of inflammatory senescence in HIV-infected persons Faced with such a complicated mechanism, what can we do to combat inflammatory senescence in HIV-infected persons? First of all, it is necessary to change bad life>
.
Second, intervene in mental health.
Subclinical depression and anxiety are common in HIV-infected people.
Mental stress can significantly increase the production of various inflammatory markers such as IL-6 and tumor necrosis factor-α (TNF-α).
Intervention and regulation of it helps to reduce the level of inflammation [25]
.
In addition, it is necessary to strengthen social support.
HIV-infected people are full of more uncertainties about aging.
Supportive social bonds can improve their physical function and mental health, improve treatment compliance, and are an important auxiliary means of HIV management
.
Third, to optimize the ART program, individualized program recommendations should be considered for the actual situation of the infected person
.
For example, as people get older, the liver and kidney metabolism of some drugs decreases.
At the same dose, exposure to drug concentrations and adverse reactions may increase, and inflammation-related mechanisms may promote inflammatory aging.
Therefore, adverse reactions should be closely monitored.
, Adjust the drug dosage or program in time
.
For example, as we mentioned at the beginning, after the elderly infected with B/F/TAF are converted to B/F/TAF, while maintaining virological suppression, it can improve treatment satisfaction and at the same time ensure the healthy quality of life of the elderly infected
.
Moreover, as mentioned earlier, during the aging process, HIV-infected senescent cells in mitochondrial dysfunction and changes in lipid metabolism lead to increased inflammation.
They need new drugs that have less impact on mitochondrial function and lipid levels, such as new drugs.
Generation INSTI
.
The picture is from veer.
com.
Fourth, to improve the composition of intestinal microbes.
Studies have found that probiotics can improve intestinal homeostasis and reduce inflammation in HIV-infected patients receiving ART [26-27].
The pilot study also showed neurological recognition.
Knowing the outcome of improvement, therefore, supplementing with probiotics to improve intestinal microbes may have clinical benefits [28-29]
.
Fifth, auxiliary anti-inflammatory and anti-aging drugs, including IL-1b or IL-6 inhibitors, as well as metformin, statins and senolytics
.
The first two target key molecules in the development of inflammation, and reduce the level of inflammation by blocking the inflammatory pathway
.
Statins are commonly used drugs for the elderly and may have the added benefit of reducing vascular and systemic inflammation
.
SATURN-HIV research has proved that rosuvastatin is related to reducing the activation of monocytes/macrophages in HIV-infected patients [30]
.
Metformin can reduce inflammatory factors, improve intestinal microbes, increase short-chain fatty acids, and reduce inflammation levels
.
Senolytics is the general term for a new class of drugs, that is, drugs that directly target and eliminate those "old but not dead" senescent cells [31]
.
In general, inflammation occurs with age and is the basis of many age-related diseases.
There are multiple mechanisms that work together.
Even HIV-infected people who insist on ART treatment are easily affected by it
.
In the future, there is much we can do in this regard, including continuing to explore the mechanism of inflammatory aging; developing new ART drugs that help inhibit inflammation, improving existing drug regimens or drug combinations; improving comprehensive disease management and increasing Comprehensive assessment of psychological, life obstacles, physical changes and drug interactions, and multilateral interventions
.
In addition, in terms of clinical research, older HIV-infected people are usually excluded from early trials.
Increasing clinical research focusing on them as the main research object will help to develop a more realistic situation for elderly HIV-infected people.
Treatment options
.
Through these improvements and efforts, greater progress will be made in extending the life expectancy and healthy life of HIV-infected persons and improving their quality of life in the future
.
Rosuvastatin reduces vascular inflammation and T cell and monocyte activation in HIV-infected subjects on antiretroviral therapy[J].
Journal of acquired immune deficiency syndromes (1999), 2015, 68(4): 396.
[31] Hickson LTJ, Prata LGPL, Bobart SA, et al.
Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease[J].
EBioMedicine, 2019, 47: 446-456.
How to manage the barriers to knowledge? Experts say so! Get more latest literature, guidelines and cutting-edge information in the fields of infectious diseases, hepatitis and AIDS-welcome to follow "Jizhiyi"-"This article is only used to provide scientific information to medical and health professionals, and does not represent the platform's position" Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease[J].
EBioMedicine, 2019, 47: 446-456.
A wonderful review of how to manage HIV-related cognitive impairment? Experts say so! Get more latest literature, guidelines and cutting-edge information in the fields of infectious diseases, hepatitis and AIDS-welcome to follow "Jizhiyi"-"This article is only used to provide scientific information to medical and health professionals, and does not represent the platform's position" Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease[J].
EBioMedicine, 2019, 47: 446-456.
A wonderful review of how to manage HIV-related cognitive impairment? Experts say so! Get more latest literature, guidelines and cutting-edge information in the fields of infectious diseases, hepatitis and AIDS-welcome to follow "Jizhiyi"-"This article is only used to provide scientific information to medical and health professionals, and does not represent the platform's position"
