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(wow) Words Of Wonders Level 2562 Answers
Why is drug resistance common and vaccine resistance rare? Both drugs and vaccines put significant pressure on pathogen populations to develop resistance, and indeed, drug resistance often appears soon after drug introduction. But vaccine resistance rarely appeared. Using well-established principles from population genetics and evolutionary ecology, we argue that two fundamental differences between vaccines and drugs explain why vaccines have so far been more robust against evolution than drugs. First, vaccines are preventive, while drugs tend to be curative. Second, vaccines tend to elicit immune responses against multiple targets of a pathogen, whereas drugs tend to target only a few. As a result, populations of pathogens produce less variation for vaccine resistance than for drug resistance, and selection has less opportunity to act on that variation. When vaccine resistance evolved, these principles were violated. With careful foresight, it may be possible to identify vaccines at risk of failure even before they are introduced.
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Pathogen evolution affects the effectiveness of vaccines and antimicrobial drugs (eg, antibiotics, antivirals, antimalarials) very differently (Figure 1). After the introduction of a new drug, drug resistance can evolve rapidly and lead to treatment failure [12]. For example, most S. aureus isolates in British hospitals were resistant to penicillin just 6 years after the introduction of the drug [13]. Similar evolutionary trajectories have been observed for the vast majority of drugs [14] and many drugs are now clinically useless against certain pathogens [15]. This problem has become so acute that drug resistance is considered one of the great challenges of our time, alongside climate change and overcoming terrorism [16]. Instead, vaccines usually provide stable disease control. Most human vaccines have continued to provide protection since their introduction decades or even centuries ago (Figure 1). For example, smallpox was eradicated because viral strains capable of transmission between vaccinated individuals never emerged [17]. In fact, the evolution of vaccine resistance is so rare that vaccines are now considered the main solution to the problem of drug resistance [11, 18].
Figure 1. Time to first detection of human pathogens resistant to vaccines [1–6] and antimicrobial drugs [7]. Similar patterns exist for antiviral drugs, although the evolution of antiviral resistance can often be delayed by the use of combination antiviral therapy [8, 9]. Viral vaccines labeled in purple, bacterial vaccines labeled in green. The blue x’s represent the first observations of resistance, with lines starting at the time of product introduction (except for smallpox vaccination, which started much earlier). Note that, in all cases, significant public health benefits extended beyond the initial emergence of resistance. Only vaccines in the current immunization schedule recommended by the Centers for Disease Control and Prevention [6] are indicated with the addition of smallpox vaccine. Global smallpox eradication (marked as a solid blue circle) has ended the opportunity for resistance to emerge (blue line). Seasonal influenza vaccine is typically attenuated by antigenic evolution, evolution occurring even in the absence of vaccination (dotted line). We consider the first occurrence of a vaccine-resistant strain of pertussis to be the first record of a protactin-negative strain [5]. This story [10] and several others (eg, [11] ) are debatable, but the overall pattern is strong: drug resistance occurs more readily than vaccine resistance.
However, both drugs and vaccines strongly suppress pathogen fitness, and therefore both must exert tremendous evolutionary pressure for resistance (defined here as a phenotype that enhances pathogen replication or survival in treated hosts). So why does pathogen evolution regularly impair the effectiveness of drugs but rarely that of vaccines (Figure 1)? Here we propose that known principles of resistance management explain why vaccine resistance rarely evolves.
Note that we limit our discussion to evolutionary changes that result from the mutation or amplification of extremely rare variants (those maintained by the equilibrium of mutational selection). This approach avoids cases of “common serotype switching,” in which strains of a pathogen previously observed but not intentionally targeted by vaccines increase after initiation of vaccination. Although serotype replacement is a form of evolution and important attention in the vaccinated host population, this process is perhaps best explained by purely ecological factors and therefore requires separate exploration [19]. To make a pharmaceutical analogy, serotype switching is analogous to an opportunistic infection, such as Clostridium difficile, that appears after using drugs to treat a different pathogen. This is certainly an important phenomenon, but it is distinct from resistance evolution because the intervention remains effective against its intended target.
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A growing body of evidence suggests that multiple human vaccine targets are evolving (e.g. [10, 20–23]), although the public health consequences of these evolutionary pathways are often unclear (e.g. [10, 22] , 24-26]). Veterinary vaccines provide additional examples, including the evolution of new serotypes [27], antigenic loss [28], antigenic drift [29, 30] and changes in life history [31, 32]. However, vaccine resistance is relatively rare and, when it does occur, it takes longer to develop than antimicrobial resistance (Figure 1).
It is well known that evolutionary trajectories are influenced by certain system details. But here’s a generality: Pathogen evolution almost always harms drugs, but rarely vaccines (Figure 1). This suggests that important features may be common to each of these classes of disease intervention. For example, it is common to associate drugs with bacterial diseases and vaccines with viral diseases, so one might wonder whether bacteria simply have the ability to develop greater resistance to viruses. But this cannot be a complete explanation: viruses quickly become resistant to antiviral drugs. For example, resistance to anti-influenza drugs [33, 34] and to the herpes virus [35, 36] appeared a few years after FDA approval, and resistance to antivirals rapidly increased in people infected with the human immunodeficiency virus. (HIV). and hepatitis C virus (HCV). patients unless they strictly follow specific treatment protocols [8, 9] (a point we will address later). Furthermore, vaccine resistance has yet to emerge in several species of bacteria (Figure 1), although drug resistance is readily emerging. Therefore, drugs cannot be more vulnerable to pathogen evolution because of the differences between bacteria and viruses. The explanation must lie elsewhere.
Previous efforts to understand the absence of vaccine resistance have focused primarily on measles. Frank and Bush [37] hypothesized that the inability of the measles virus to escape vaccination may be due to a rapid trade-off between rapid pathogen transmission and antigenic flexibility. However, one might wonder why selection did not compensate for this antigenic plasticity when mass vaccination began to lead to local extinction. Calland et al [38] suggested that the measles virus may have an unusually low mutation rate for an RNA virus, but Schrag et al. [39] showed that measles virus mutates at a rate similar to other RNA viruses. Fulton et al [40] showed that measles virus antigens can be strongly constrained by natural selection, but in the same paper they also showed that evolutionary restriction is weaker for influenza virus antigens, suggesting that although antigenic restriction may be a feature of the measles virus, it is not. Intrinsic characteristics of vaccine targets
We are aware of only one attempt to find a general explanation of why vaccine resistance is rare. McLean [41, 42] noted that vaccines against childhood diseases such as measles, polio, and smallpox mimic the natural immunity that evolutionary pathogens have failed to avoid despite strong selection for at least thousands of years (indeed, it is by this is called childhood immunity). diseases: is limited to non-immune people). He argues that natural and vaccine-induced immunity to these diseases are robust against evolving pathogens because they are “largely cross-reactive.” This raises the question of what exactly is meant by reciprocity in the broadest sense. Antimicrobials are also largely cross-reactive, in the sense that they also kill a wide range of strains, but drug resistance easily evolves.
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Here, we argue that vaccines are less vulnerable to pathogen evolution than antimicrobials because of differences in how drugs and vaccines work. We argue that two main features of vaccines have large synergistic effects on the rate of emergence of resistance and subsequent spread (Table 1, formalized in electronic supplemental material, appendix). Our hypothesis is amply supported by experimental and theoretical work designed to slow the evolution of drug resistance [43]. Elements of what we propose have been hinted at previously (eg, [11, 42, 44-46]), but, to the best of our knowledge, our argument has never been fully developed.
Table 1. Summary of our reasoning. In most cases, vaccines act quickly and produce immunity that serves multiple purposes. These features reduce the likelihood of resistance developing in the first place and, if it does, slow the spread of resistance.
For most infectious diseases, hours or days elapse between exposure to a pathogen and symptomatic infection in the host. Normally, a relatively small number of virions or pathogenic cells cause infection, but as they continue to replicate, populations increase until they reach relevant numbers.
