However, people living with HIV who have a lower CD4 count where some damage to the immune system has occurred sometimes also experience reductions in the numbers of certain other cells in their blood. Some of these problems may be caused by damage to the bone marrow where blood cells are produced. HIV can damage the bone marrow by infecting its cells directly, or by disrupting levels of natural chemicals called growth factors that help bone marrow cells develop. The bone marrow may also be affected by some drugs or the illnesses that can develop if you have a weak immune system opportunistic infections. A decrease in blood cells can also be caused by the destruction of cells in the circulation or by bleeding disorders such as haemophilia.
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- I did another test after a month of previous test after 15 days which is around last of 5th month, cbc test wbc was im shocked wbc was decreased so much I did another test on exact 6 month after 24 days of 1St hiv test it was Elisa 4 gen and came negative..
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- White blood cells or leucocytes play a crucial role in our body.
HIV-induced changes in cytokine responses to bacteria may influence susceptibility to bacterial infections and the consequent inflammatory response. We examined the impact of HIV on whole blood responsiveness to bacterial stimulation in asymptomatic subjects and patients with bacterial bloodstream infection BSI.
Whole blood was stimulated ex vivo with two bacterial Toll-like receptor agonists lipopolysaccharide and lipoteichoic acid and two pathogens Streptococcus pneumoniae and non-typhoidal Salmonella , which are relevant in HIV-positive patients. These results suggest a complex effect of HIV on leukocyte responses to bacteria.
However, in patients with sepsis, leukocyte responses were equally blunted in patients with and without HIV infection. HIV patients have an increased risk of developing bacterial bloodstream infections BSIs and sepsis, which are associated with higher mortality [ 1 — 4 ]. Although the immunological mechanisms behind enhanced susceptibility, morbidity and mortality due to bacterial infections in HIV patients are incompletely understood, previous studies suggest a role for inadequate release of soluble mediators such as cytokines [ 5 ].
Pro-inflammatory cytokine release is an essential element of the host response during bacterial infection, which is important for protective immunity but also causes collateral damage due to exaggerated inflammation [ 6 ]. Sepsis is also associated with immune suppression, which involves a reduced ability of leukocytes to respond to re-stimulation with bacterial agonists [ 7 , 8 ].
In contrast, previous investigations suggested that HIV infection results in priming of leukocytes to stimulation with bacterial agonists. Knowledge on the impact of HIV infection on the responsiveness of whole blood leukocytes to bacterial stimuli is limited, especially in the HIV endemic setting of sub-Saharan Africa.
This information is relevant to understand host defences against bacteria in HIV patients and to obtain insight into the effect of HIV infection on hyper-inflammation and immune suppression during sepsis. Therefore, we examined 1 the whole blood leukocyte response in asymptomatic patients with HIV compared to healthy controls and 2 whether HIV co-infection influences sepsis-induced suppression of leukocyte responses to a secondary stimulus.
The cohort reported here was featured in part in previous studies on the impact of HIV infection on presentation and outcome of febrile illness, activation of the complement system and neutrophil extracellular traps [ 4 , 14 , 15 ]. Patients were included in the present analysis as soon as the blood culture became positive; at that moment, a second blood sample was drawn for whole blood stimulation as described below.
Afebrile, asymptomatic controls, with or without HIV infection, were recruited in the vicinity of the hospital and the HIV outpatient clinic. Written informed consent was obtained from all participants or their guardians. Coagulase-negative staphylococci and Bacillus spp. Streptococcus viridians were regarded as contaminants as well, unless the patient had clinical signs of endocarditis or meningitis.
As part of a clinical trial requirement, the microbiology laboratory at the Albert Schweitzer Hospital successfully participates in regular external quality assurance programmes addressing species identification. Glomerular filtration rates were estimated by the modification of diet in renal disease MDRD formula [ 16 ]. Stimulations in BSI patients and controls were done on one occasion. Asymptomatic subjects were sampled on inclusion into the study.
To establish the optimal dose of heat-killed bacteria, LPS and LTA, to induce a robust cytokine response, we performed whole blood stimulations with serial dilutions of stimuli, using blood from healthy volunteers. Each cytokine assay was done for all samples in one run on the same day using the same batch of reagents, thereby eliminating inter-assay variability. Categorical variables are presented as percentages and continuous variables as medians with their interquartile range in the table and as box-and-whisker plots in the figures.
We used Fisher's exact tests for comparisons of categorical variables, Mann—Whitney U tests or Kruskall—Wallis tests to assess differences for non-normally distributed continuous variables, and unpaired t -tests or one-way ANOVA tests for normally distributed variables. Cytokine release in response to a stimulus was determined by calculating the difference in cytokine levels between the stimulated and medium control samples. Outliers were determined using a Grubbs test.
Samples with outliers in the unstimulated control were excluded from our analyses. An additional sensitivity analysis was performed in some cases to correct for differences in leukocyte count by dividing cytokine read-outs by the number of leukocytes.
This was an exploratory study, so a formal sample size calculation could not be performed. No mathematical correction was made for multiple comparisons. Table 1 presents the baseline characteristics of the study population. In addition, we obtained blood cultures from patients, 33 of which revealed a bacterial pathogen, including 14 patients with HIV infection.
Data are presented as medians interquartile ranges , except for sex, renal failure, liver injury and antibiotic treatment; p -values below 0. The causative pathogens are depicted in Table 2. There were no differences in pathogens according to HIV status, except for infection with S. Two asymptomatic HIV patients had to be excluded from analysis due to outliers in the unstimulated control samples.
Cytokine releases from unstimulated whole blood medium control samples are depicted in Figure 1. Spontaneous cytokine release by whole blood samples from BSI patients and asymptomatic subjects with or without HIV infection.
Whole blood was kept in RPMI medium for 24 hours. Data are depicted as box-and-whisker plots depicting the smallest observation, lower quartile, median, upper quartile and largest observation. Significant differences between HIV-negative asymptomatic controls and asymptomatic HIV patients or sepsis cases are shown, as well as differences within groups asymptomatic or sepsis according to HIV status.
To examine whether this finding was related to lower leukocyte counts in asymptomatic HIV patients, a sensitivity analysis was performed in which results were corrected for leukocyte counts.
Whole blood was stimulated for 24 hours. The capacity of leukocytes to respond to bacterial agonists is a strong denominator of both the early protective immune response and the late, potentially damaging inflammatory reaction. In addition, the reduced ability of leukocytes to react to bacterial agonists during established severe infection has been implicated as an important feature of immune suppression in patients with sepsis [ 7 ].
We hypothesized that HIV infection might influence the cytokine production capacity of blood leukocytes and studied this in asymptomatic subjects and patients with BSI. HIV infection had no influence on the diminished cytokine production capacity of blood leukocytes from BSI patients.
Our findings extend the relevance of these findings to a whole blood stimulation model and a wider range of bacterial agonists. Several mechanisms could be involved in reduced NK cell responsiveness in HIV patients, including the expansion of an unresponsive subset of NK cells and shedding of MHC class I chain-related molecules, which provide negative feedback to NK cells [ 5 ].
We observed no significant differences in whole blood leukocyte responses between asymptomatic patients with and without cART. A possible explanation for the absence of improvement on cART is the presence of more advanced disease in patients on cART, as illustrated by their lower CD4 counts Table 1.
However, we did observe consistent priming of pro-inflammatory cytokine release after stimulation with NTS in asymptomatic HIV patients without cART as compared to healthy controls. In line with this finding, a previous study found that HIV infection was associated with enhanced cytokine release from alveolar macrophages in response to NTS [ 22 ]. The enhanced susceptibility of HIV patients to invasive NTS suggests that enhanced pro-inflammatory cytokine release upon NTS exposure is not protective, but may contribute to more extensive tissue damage.
In patients with BSI, HIV co-infection had no impact on the capacity of blood leukocytes to release cytokines, regardless of the cytokine read-out or stimulus applied. In line with this, we observed a predominantly common genomic response of whole blood leukocytes in Dutch ICU patients with or without sepsis [ 24 ]. These results suggest a predominantly common host response in sepsis patients with or without HIV co-infection. Our study was limited by the relatively small number of patients with BSI, so we grouped patients with different pathogens and sites of infection.
Possibly as a consequence, variance in leukocyte responses within groups was relatively large. Differences in antibiotic treatment regimens was another potential source of variance. In order to avoid a type I error, we did not correct for multiple comparisons. However, by testing different bacterial stimuli and different read-outs, we were able to observe consistency in leukocyte responses in different patient groups. To the best of our knowledge, this is the first study to examine the impact of HIV on leukocyte responsiveness in patients with BSI.
This work was financially supported by the foundation De Drie Lichten in the Netherlands. We thank Becton Dickinson for providing blood culture bottles free of charge for this study; Richard Molenkamp for his assistance in determining viral loads Department of Virology, Academic Medical Center, Amsterdam, Netherlands ; Dr.
We declare that none of the authors have any conflicts of interest. All authors discussed the results and implications and commented on the final version of the manuscript. National Center for Biotechnology Information , U. Published online May Author information Article notes Copyright and License information Disclaimer. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article has been cited by other articles in PMC. Abstract Introduction HIV-induced changes in cytokine responses to bacteria may influence susceptibility to bacterial infections and the consequent inflammatory response.
Methods We examined the impact of HIV on whole blood responsiveness to bacterial stimulation in asymptomatic subjects and patients with bacterial bloodstream infection BSI. Conclusions These results suggest a complex effect of HIV on leukocyte responses to bacteria. Keywords: HIV, sepsis, cytokines, innate immunity, bacterial infections, leukocyte reprogramming. Introduction HIV patients have an increased risk of developing bacterial bloodstream infections BSIs and sepsis, which are associated with higher mortality [ 1 — 4 ].
Whole blood stimulation and assays Stimulations in BSI patients and controls were done on one occasion. Statistical analysis Categorical variables are presented as percentages and continuous variables as medians with their interquartile range in the table and as box-and-whisker plots in the figures. Results Patient characteristics Table 1 presents the baseline characteristics of the study population. Table 1 Baseline characteristics of the study populations. Open in a separate window.
Percentages were calculated using the total number of patients for whom data was available. Table 2 Sites of infection and causative pathogens in patients with bloodstream infection. P -values below 0. The single HIV-positive patient in this group was infected with a group C streptococci. Figure 1. Figure 2. Discussion The capacity of leukocytes to respond to bacterial agonists is a strong denominator of both the early protective immune response and the late, potentially damaging inflammatory reaction.
Conclusion To the best of our knowledge, this is the first study to examine the impact of HIV on leukocyte responsiveness in patients with BSI. Acknowledgements This work was financially supported by the foundation De Drie Lichten in the Netherlands. Competing interests We declare that none of the authors have any conflicts of interest. References 1. Community-acquired bacterial bloodstream infections in HIV-infected patients: a systematic review.
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Reducing the viral load to "undetectable" levels slows or stops disease progression and prevents HIV transmission to sex partners. Acute HIV symptoms usually appear between weeks post exposure, and only last for a couple weeks at most. These are reported as a percentage of the WBC. Conditions and Diseases Risks. Very low readings of RBC values can indicate anemia , a condition wherein cells and tissues are not provided ample supplies of oxygen. They fight infections by "eating" germs and telling the immune system what germs they have found. You marked this post as helpful!
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However, people living with HIV who have a lower CD4 count where some damage to the immune system has occurred sometimes also experience reductions in the numbers of certain other cells in their blood. Some of these problems may be caused by damage to the bone marrow where blood cells are produced. HIV can damage the bone marrow by infecting its cells directly, or by disrupting levels of natural chemicals called growth factors that help bone marrow cells develop.
The bone marrow may also be affected by some drugs or the illnesses that can develop if you have a weak immune system opportunistic infections. A decrease in blood cells can also be caused by the destruction of cells in the circulation or by bleeding disorders such as haemophilia. Apart from a decline in CD4 cells, the three most common blood problems among people living with HIV are anaemia, neutropenia and thrombocytopenia. They are all detected using standard blood tests that you should have as part of your normal HIV care.
Anaemia means a shortage of red blood cells. Red blood cells transport oxygen around the body, so anaemia can cause symptoms of tiredness and breathlessness. It can be a side-effect of zidovudine, although it is rare among people with CD4 counts above Zidovudine is now rarely used if you are starting HIV treatment. If you are taking zidovudine and develop anaemia you may be able to change to a different drug.
But zidovudine is an important drug option for some people, particularly during pregnancy. To treat anaemia, doctors can prescribe an injected drug called erythropoietin.
This stimulates the body to produce more red blood cells. People with severe anaemia may need blood transfusions to top up their red blood cells. If the anaemia was caused by taking a drug, after the anaemia has been treated it may be possible to resume taking the drug, this time at a lower dose. Anaemia can also be caused by some opportunistic infections. If these are treated, the anaemia normally improves.
Anaemia can have other causes, unrelated to HIV and drug treatments. Iron deficiency is a common cause of anaemia in the UK. It is often caused by bleeding, for example from a stomach ulcer or heavy periods. It is also quite common in pregnancy. If you are diagnosed as having iron deficiency anaemia, your doctor may recommend supplements or changes to your diet. Neutropenia means a shortage of neutrophils.
These are a type of white blood cell that mainly attack bacteria and fungi, so people who have neutropenia are at increased risk from these infections. The most common cause is the anti-HIV drug zidovudine, the anti-cytomegalovirus CMV drug ganciclovir or drugs used to treat cancers and tumours. People living with HIV often have slightly lower levels of neutrophils than people who don't have HIV, but serious neutropenia is rare among people with CD4 counts above Neutropenia can be treated by stopping the drug which is causing it or reducing the dose.
Alternatively, if the neutrophil count falls very low below doctors may prescribe G-CSF granulocyte-colony stimulating factor , a drug which stimulates the body to produce white blood cells and has been shown to improve neutropenia and reduce the risk of infections.
Both of these drugs are given by injection. A shortage or change in the size or function of red blood cells. These cells carry oxygen to organs of the body. Symptoms can include shortness of breath, fatigue and lack of concentration. A shortage of neutrophils, a type of white blood cell that fights bacterial infections. A decreased number of specific cells in the blood responsible for blood clotting.
Thrombocytopenia means a shortage of platelets, which are cells that help the blood to clot. People who have thrombocytopenia may bruise very easily or, in serious cases, develop uncontrollable bleeding. HIV can infect the cells in the bone marrow that produce platelets. HIV can also confuse the immune system into attacking platelets in the circulation and removing them using the spleen.
Thrombocytopenia can also be caused by drugs such as ganciclovir. If it is caused by other treatments, it is treated by reducing their dose or using other drugs. Some cases may be treated using mild doses of steroids or intravenous immunoglobulin. Greta Hughson. November Some of these problems may be caused by damage to the bone marrow. These problems include anaemia, neutropenia and thrombocytopenia.
Glossary anaemia A shortage or change in the size or function of red blood cells. Next review date. This page was last reviewed in November It is due for review in November Related topics.
Low CD4 count.